Guide To Internal Medicine (How To Get Honors!)

hey welcome to my guide to internal

medicine for third year medical students

i'm going to be going over all the

high-yield pim questions that you're

most likely to get asked on this

rotation and also the most important

information that you need to know in

order to get honors this is going to be

applicable to both internal medicine and

family medicine because there's a lot of

overlap and we have a lot of material to

cover so i will be going pretty quickly

but hopefully you can review things or

leave a question in the comments below

if you need further clarification first

of all i'd like to start off with six

questions that you can ask patients at

any time while they're in the hospital

and for internal medicine it's basically

just kind of a review of systems did you

have any fevers or chills overnight any

chest pain shortness of breath abdominal

pain nausea and vomiting and did you

have a bowel movement and then one bonus

question is that i really like asking

about patients hobbies i feel like this

is a very underrated question to ask but

it immediately helps you build rapport

with your patients because they feel

like you're expressing interest in them

and sometimes you actually do really

find useful information with this

question as well next are three

additional things i wanted to talk about

is that one don't underestimate the

review of systems i feel like in medical

school i didn't think the review of

systems was that useful but now as a

resident i've come to realize the

strength and how useful it is when you

really don't know what's going on just

doing a full head to toe systems review

can sometimes really clarify what's

actually going on with the patient and

then all patients need a med wreck on

admission or med reconciliation that's

because internal medicine and in family

medicine patients are on a lot of

medications and so you we need to go

through all of the medications and

ensure that we know exactly what meds

they're taking at home so that we can

properly give them the meds that they

need while they're in the hospital so as

a medical student this is one of the

most important and helpful things that

you can do for your residents is doing a

thorough med wreck because it's a very

time consuming process and it's actually

very helpful when a medical student can

do that and that can be very helpful for

your team and then finally

social history is really important and i

think this is also something i

underestimated during medical school but

knowing where a patient lives what their

baseline functional status is like are

they able to ambulate on their own or do

they need a cane or a walker these are

very important questions to know early

on because it helps you plan for where

the patient is eventually going to

discharge to or what we call dyspo

so let's just get right into it there's

a huge

number of different conditions that i

basically came up with off the top of my

head that we see frequently in internal

medicine but i'm just going to kind of

choose the high-yield ones that are most

important and that you're most likely to

encounter on your rotation in internal

medicine so first one it's going to be

atrial fibrillation this is the most

common arrhythmia and just getting

straight into it i like to teach medical

students a mnemonic for causes of atrial

fibrillation and that mnemonic is the

pirate's mnemonic so p is for pulmonary

or postop i is for ischemia for example

acute coronary syndrome r is rheumatic

heart disease a is anemia t is thyroid e

is electrolytes and ethanol and s is for

sepsis so these are some of the most

common causes of atrial fibrillation and

what are the two major complications of

atrial fibrillation so why do we care so

much about if a patient has atrial

fibrillation what are the bad things

that can happen in patients with this

and the one that you really need to know

as a medical student is that afib is

really a huge risk factor for stroke

and then the other complication you

should know about is what's called rvr

or rapid ventricular response where your

heart will start just beating very

rapidly and this can cause hemodynamic

compromise but definitely you need to

know that stroke is the big thing we're

worried about with atrial fibrillation

and what is the location that thrombi

typically form

so what happens in atrial fibrillation

is your atria are just kind of

fibrillating and so the blood kind of

pulls there and is very stagnant and so

you get a blood clot and eventually that

blood clot can shoot off go into your

blood vessels go into your brain and

then cause a stroke so that's how it

works and one common pimp question

you'll be asked is where do these blood

clots form and the answer's hat is going

to be the left atrial appendage

what is a score that we can use to

estimate the risk of stroke this is very

huge and something i didn't know when i

was a third year medical student going

into my internal medicine rotation but

this is going to be the chad's vasc

score and you definitely need to know

this because it's going to come up a lot

and basically we calculate a risk of

stroke based on several risk factors for

example congestive heart failure

hypertension age greater than 65

diabetes stroke vascular disease age

greater than 75 and sex category

basically meaning if you're female you

get an extra point and if your score is

greater than two that is usually an

indication to anticoagulate or put a

patient on a blood thinner to prevent

the risk of stroke

and then on the flip side we have a

score that estimates the risk of

bleeding if we do start a blood thinner

or anticoagulation and that's going to

be the has bled score but in terms of

the scores you need to know you

definitely definitely need to know the

chad's fast score

what medications do we use to treat

atrial fibrillation so as i mentioned

before we use a blood thinner um but the

other one that we use is kind of to

prevent this rvr

and that's going to be rate control

medications so the two main classes of

medications rate control medications

like beta blockers and calcium channel

blockers and blood thinners like

warfarin or rivaroxaban apixaban things

like that

so a couple landmark trials if you can

know these trials and talk about them

during rounds you're going to look like

an all-star in front of your team and in

front of your attendings and that can

really help you get honors but there's a

landmark trial that showed that rate

control is equal to rhythm control and

that was called the affirm trial and

basically the reason we favor rate

control is because the rhythm control

actually had a trend towards increased

mortality and they had uh higher side

effects so usually we start with rate

control and then another important trial

that showed that going for a lenient

rate control goal of heart rate less

than 110 is better than strict heart

rate control less than 80 is the race 2

trial and so these are two trials that i

think if you can say in front of your

team you're going to really you know

impress your team overall next let's

talk about treatment for afib in a

patient who is hemodynamically unstable

so when anybody who is unstable blood

pressure 60 over 40 they're in rapid

afib with rvr the answer to this is

going to be cardioversion you're just

directly going to shock them out of the

rhythm

and then if a patient has prolonged afib

with rvr and then they start to develop

congestive heart failure from this what

is that called this is a pimp question

that i got as a medical student and

that's called tachycardia mediated

cardiomyopathy

next let's move on to acute coronary

syndrome and there are three different

types of or classifications of acute

coronary syndrome that you should know

and that's going to be

unstable angina n-stemi and stemi and

the big thing is that you need to know

what differentiates unstable angina from

n-stemi and stemi and so unstable angina

is going to see no elevation in the

troponin level whereas n-stem and stemi

do and this is a little graphical

depiction of some of the differences

unstable angina and stemi and stemi

the big difference you see here unstable

agina you do not have a troponin

elevation

how long does it take before troponin

starts to rise after an mi this is

another common question that you might

get but it actually takes about four

hours for troponin to rise and this is

why if somebody acutely comes in with

chest pain after like an hour they may

have a negative troponin and if their

history is concerning enough you're

gonna be trending ekgs and troponins

just so you make sure you don't falsely

discharge somebody because they have a

negative troponin it may just not have

peaked or

risen yet and then what treatment should

immediately be given if suspicious for

mi that's going to be aspirin 325

milligram load and then 81 milligrams

daily uh other treatments we often give

is going to be a lipid

lowering agent like a torvastatin and

anticoagulation like heparin and then

what are the three different types of

treatments for mi this is basically

going to be we can do medical management

for it or we can do a stent or also

known as pci

where we go in and deploy a stent that

opens up the blockage in the blood

vessel and then finally we can do

surgical intervention with a cabbage a

coronary artery bypass graft and then

what history finding is most specific

for a qmi this is actually going to be

radiation of pain to the right arm

typically we learned that the pain will

radiate down the left arm but actually

studies have shown that if a patient

reports pain radiating down the right

arm that's actually more specific for mi

compared to the left side and this is a

trick question you might get on your

rotation uh if a patient has chest pain

with tenderness to palpation of the

chest wall or if it's reproducible with

palpation of the chest wall this is code

for

thinking that it's something

musculoskeletal or costochondritis and

so if somebody's having acute coronary

syndrome they shouldn't get pain with

palpation to their chest wall and then

there are three features of typical

chest pain that you should know about

that's going to be

substernal chest pain that's worse with

exertion and relieved with rest or

nitroglycerin and the reason it's

important to know these three typical

features is because we have some

different definitions so

if you meet three out of three of these

criteria that's called typical chest

pain if you meet two out of three that's

called atypical chest pain and then if

you meet

zero to one out of three that's called

non-cardiac chest pain

okay and so that's what the answer to

this question is right here

finally if a patient has elevated

troponins and signs of ischemia but you

don't think it's from acute coronary

syndrome what do we call this so say

somebody is in septic shock their blood

pressure is 70 over 40 they've been

hypotensive all the time

febrile and just really sick and they

have elevated troponins the answer to

this is going to be what we call a type

2 mi or what is also known as demand

ischemia and i remember as a medical

student people would throw this term out

and i didn't really know what they were

talking about but this is what they mean

when they have they're having an

infarction they're having elevated

troponins but it's not due to a primary

acs event

next let's talk about copd one of the

most common diagnoses we're going to be

treating in the hospital so there are

only two treatments that reduce

mortality in copd and this is an

important question that you're likely to

get asked and that's going to be oxygen

supplementation and nicotine cessation

so stopping smoking is very important

what is the goal oxygen saturation in

these patients that's going to be a goal

o2 sat of 88 to 92 percent

and the reason we don't aim for a higher

goal is that giving patients with copd

too much oxygen is actually a bad thing

and why is it bad this is another common

question you might get and uh what a lot

of people will tell you is oh it's

because copd patients start to use

hypoxia as a drive of their respiratory

rate rather than

you know us without copd we use carbon

dioxide to determine our respiratory

rate so too much oxygen will cause

decreased respiratory drive that's the

most common answer people will give but

the real reason is actually not

decreased respiratory drive the real

reason is actually reversal of hypoxic

pulmonary vasculature and that sounds

very confusing but i'm going over this

because this is going to be on your

board exams it's going to be on your

shelf exams and you're going to get

pimped about this and the real answer is

reversal of hypoxic pulmonary

vasculature so basically in copd you

have areas that are obstructed and that

are not well ventilated so what happens

is you have blood vessels going to those

areas and the copd patients will

constrict blood vessels there to reduce

blood flow to places with poor

ventilation now if you give tons of

oxygen to this patient and now they're

setting 100 percent well

now these blood vessels are going to

dilate because there's sufficient oxygen

in those areas but those places still

have very poor gas exchange because

they're still obstructed and poorly

ventilated and this can actually cause

paradoxically them to go into

respiratory failure

so what is the typical progression of

inhaled treatments for copd this is a

really nice one to know just to know

like how severe somebody's copd is so

for copd we usually start with a

long-acting muscarinic antagonist like

teotropium and then we move on to a

long-acting beta agonist like salmeterol

and then finally inhaled corticosteroids

interestingly for asthma we do basically

the exact opposite so we start off with

an inhaled corticosteroid then we go to

a laba and then we go to a llama

and the other thing is that all of these

patients should have a short acting beta

agonist like albuterol

ordered for prn use when they're having

wheezing or feel like they're having a

bit of a flare

what are the criteria that define a copd

exacerbation there's going to be two

main criteria that we look for and

that's going to be change in sputum

either the amount or the quality and

then increasing dyspnea or shortness of

breath and then what is a nebulized

treatment that we often give in the

hospital for acute exacerbations that's

going to be what's called a duoneb and

i'm just putting this here because you

know we hear we throw this term all out

all the time but what it really is is

iprotropium and albuterol so this is a

short-acting muscarinic antagonist and

this is a short acting beta agonist

what medications do we give to actually

treat the copd exacerbation the answer

to that is going to be steroids and

azithromycin and how long do we give

steroids that's going to be five days

and this is based on the reduced trial

which compared five days of steroids

versus 14 days of steroids and found

that the five-day group actually had

better outcomes and then why is

azithromycin often useful for copd

exacerbations the answer to this is that

it's thought to decrease inflammation in

the airways and really help recovery

during a copd exacerbation and then what

is the indication to start oxygen in

copd so say somebody has copd but

they've never been on oxygen before when

do you decide to start oxygen at home

for them and that's going to be if their

oxygen saturation is less than 88

or if their pao2 is less than 55. and

then this is another important question

not only for real-life scenarios but

this comes up on the boards a lot but

say there's an asthma or copd patient

who starts to look worse but when you

listen to them on physical exam their

wheezing is actually gone now and their

pco2 rises to 40 which is kind of the

normal value of your carbon dioxide the

answer to this

you know what's going on here is that

they have impending respiratory failure

okay so you notice that they're looking

worse but the reason they're wheezing

goes away that does not mean they're

improving that actually means that

they're moving such little air at this

point that you don't hear the wheezing

anymore because they have such low

airflow at this point and so these

patients are going to be very dangerous

and may be needing intubation soon

and then what is a type of non-invasive

ventilation that you can use before

intubation that's going to be bipap and

i just want to let you know this is

important because bipap is different

from cpap bipap provides ventilation

which means it can blow off carbon

dioxide

okay but cpap only gives oxygenation it

does not give any ventilation so it has

no effect on the pco2 and oh and one

more question what is the fev1 to fvc

ratio that defines obstructive lung

disease you might get asked this and the

answer to that is going to be an fev1

fec ratio less than 0.7

now let's move on to cirrhosis so what

are the complications of cirrhosis

there's a whole slew of complications

and it's going to be hepatic

encephalopathy ascites spontaneous

bacterial peritonitis a varicella bleed

or hepatorenal syndrome and then any

patient that comes into the hospital

with one of these complications is said

to have what kind of cirrhosis we call

that decompensated cirrhosis so triggers

for decompensated cirrhosis the most

common trigger is going to be medication

non-adherence but there's definitely a

lot of other uh possible causes

infections and bleeds are definitely

ones we need to rule out and even even

electrolyte abnormalities and over

diuresing somebody can cause somebody to

go into decompensated cirrhosis and so

what is our main treatment for hepatic

encephalopathy that's going to be

lactulose titrated to two to three bowel

movements per day this is something that

frequently is going to get asked on your

medicine rotation how much do we want

patients to be pooping when they're on

lactulose and then you can also add

rifaximin if a patient is refractory and

then another thing that i wanted to add

is another frequent pimp question is

what is the mechanism of action of

lactulose and so what happens is

lactulose is a sugar and it gets

digested by bacteria in your gut and

when they digest it they actually

release acid into your colon and helps

acidify the colon and what happens after

your colon is acidified there's more h

plus ions around and so ammonia which is

nh3

will get turned into ammonium nh4 plus

which is not absorbed by the colon and

so

basically you're reducing the total body

amount of ammonia because you're making

it into this like non-absorbable form in

the gut by acidifying the colon so

another important question that you

might get pimped on during your medical

school rotation so what are the

different stages of hepatic

encephalopathy that's going to be stage

one which is just characterized by sleep

disturbance and then two to three is

when you start getting asterixis and you

also start to get confusion and then

four would be if a patient is basically

comatose

what is the treatment for ascites so

really we're going to have one

medication treatment and then one kind

of procedural treatment the medication

is going to be spironolactone and

furosemide in a five to two ratio this

is important ratio to know so usually

you'll see something like 50 milligrams

of spironolactone and 20 of lasix or 140

something like that and then

procedurally we can do what's called a

large volume paracentesis if a patient

is very distended and very symptomatic

so any patient with ascites and fever

needs to be ruled out for what condition

the answer to that is going to be sbp

spontaneous bacterial peritonitis and

then there are two types of paracentesis

this is a pimp question that i got wrong

during my medical school rotation

and that's going to be a diagnostic

paracentesis and a therapeutic one so

diagnostic is when you're just going to

be taking like 50ccs out of their

abdomen to make sure they don't have

spontaneous bacterial peritonitis

therapeutic is going to be you're taking

like five like 10 15 liters out to kind

of treat symptoms from how much fluid is

in their belly okay what are the

diagnostic criteria for diagnosing sbp

in acidic fluid this is a very important

question that you're very likely to get

asked but what we're looking for is pmns

or neutrophils greater than 250 and if

you see that then you can diagnose sbp

next question is how can you tell if a

city's fluid is from portal hypertension

or another etiology another pimp

question that i got wrong during medical

school but this is going to be the sag

that we've learned about the serum

ascites albumin gradient and basically

you just look at the albumin value in

their blood and compare it to

the albumin value in their ascites and

if it's a large gap greater than 1.1

that indicates a portal hypertensive

etiology here's a nice little table here

that shows that sag greater than 1.1 is

going to be your cirrhosis and portal

hypertension etiologies and then sag

lesson 1.1 is going to be nephrotic

syndrome

malignancy pancreatitis tuberculosis all

of these things here

next what is the treatment for a varicel

bleed that's going to be octreotide

ceftriaxone and a proton pump inhibitor

and you also need to make sure that they

have two large bore ivs and that you

consult gi for possible banding or

clipping off of those variceal veins and

then beta blockers is only going to be

used for prophylaxis so you don't use it

in the acute setting when they're

bleeding because they need to have some

compensatory tachycardia so beta

blockers is only after everything's

stabilized and then you add beta

blockers to prevent future bleeds next

is a very important question you might

get asked is what is a procedure that

can reduce the risk of a varicel bleed

by decreasing portal pressure that's

going to be the tips procedure and

basically what this does is you're

bypassing the liver and you go into the

hepatic vein and just bypass it and go

straight into the ivc and that reduces

portal pressure and reduces your risk of

variceal bleed the problem with tips and

this is another common question you'll

get asked or pimped on is that there is

a there's a complication that usually

gets worse with tips and that's a

worsened hepatic encephalopathy so

imagine you're now shunting everything

away from the liver and so it's not

processing and it's not getting rid of

the ammonia you're going to have higher

levels of ammonia in your body and then

get worse in hepatic encephalopathy more

on cirrhosis so is ast and alt a marker

of liver function the answer to that is

no this is a marker of liver damage and

inflammation but not function so even

though we call it the liver function

test there's actually more useful

markers of liver function and the

transaminases themselves are not really

a marker of liver function what are the

actual measures of liver function that's

going to be your pt and inr because

remember your liver helps make all those

coagulation factors your bilirubin your

albumin and your platelet level

and then what what is the score that is

used to determine the degree of

cirrhosis and the need for transplant

that's going to be the meld sodium score

another important score that you should

know about and basically if this score

is greater than 15 that's when you start

thinking about transplant for these

patients

now let's talk a little bit about acute

liver injury so there are two patterns

of liver injury that you really need to

know two broad categories of liver

injury and the reason it's important to

know this is because there's a different

differential diagnosis for both of these

so you have a hepatocellular pattern of

liver injury and a cholestatic pattern

and hepatocellular is going to be your

ast and alt uh significantly elevated

and then your alk foss and billy are

only kind of mildly elevated and then

the opposite pattern is going to be seen

with cholestatic where you have more of

a predominant aop and a billiard

elevation and a lower ast alt elevation

what are the main conditions that can

cause ast and alt in the thousands

another common pim question the way i

remember this is a vade because there

was actually a doctor at my medical

school called dr vade

and her name was basically a good

mnemonic uh which is viral hepatitis can

cause astn alt in the thousands

autoimmune hepatitis ischemic or shock

liver and then drug induced which is one

of the most common causes and then what

is an antibody for autoimmune hepatitis

you should definitely know this this is

going to be the anti-smooth muscle

antibody and an antibody for primary

biliary cholangitis this is going to be

the anti-mitochondrial antibody and then

what is the criteria for defining acute

liver failure there's actually only two

criteria that you need and that's going

to be encephalopathy and an inr greater

than 1.5 and if somebody meets the

criteria for acute liver failure then

you need to consider if they need

emergent transplant

now let's move on to congestive heart

failure so what are the different

classifications of chf so we have

systolic heart failure also known as

heart failure with reduced ejection

fraction heart failure with moderately

reduced ejection fraction and diastolic

heart failure with preserved ejection

fraction and basically if we want to do

a quick review systolic is when you're

going to have that eccentric hypertrophy

so you have a really thin left ventricle

and it just kind of balloons out and

gets really weak and doesn't contract

very well whereas diastolic is you're

going to get hypertrophied

left ventricle and it becomes very tight

and very difficult to fill and so both

of these are going to cause decreased

cardiac output and lead to heart failure

symptoms so again this is going to be

eccentric and then diastolic heart

failure is concentric hypertrophy and

what are the ejection fraction cutoffs

for the above conditions so systolic

heart failure is going to be an ef less

than 40 percent moderately reduced ef is

going to be 40 to 50 percent and

preserved ef is going to be greater than

50

and we're going to go over this in a

second but it's important to know these

different cutoffs because the treatments

actually vary based on whether they have

systolic heart failure or diastolic

heart failure so there are two broad

categories of why somebody may have

systolic heart failure and that's going

to be ischemic versus non-ischemic

cardiomyopathy so ischemic is going to

be the person with hypertension smoking

obesity diabetes and they have a heart

attack and now they have a weakened

heart muscle and that's why they have

systolic heart failure non-ischemic is

typically going to be people who are

doing drugs and get a non-ischemic

cardiomyopathy or people with viral

cardiomyopathies and now have decreased

function from that this is a little bit

above medical student knowledge but the

reason this is important is also because

our treatment approaches to ischemic

versus non-ischemic cardiomyopathy also

differs pretty much based on what the

etiology of their heart failure is and

now the next questions are going to get

to why we define systolic heart failure

versus diastolic heart failure so there

are treatments with mortality benefit in

systolic heart failure and you are

definitely going to get pimped about

this

but the answer to that is going to be

beta blockers ace inhibitors and

spironolactone and then also if you want

to go above and beyond sglt2 inhibitors

icds cardiac resynchronization therapy

and bi-dil in african-american

populations have also shown to have

mortality benefit and then on the flip

hand what are treatments with mortality

benefit in diastolic heart failure the

answer to that is actually going to be

none okay that's what your attendings

are going to be looking for when they're

pimping you on this question and that's

not entirely true because there are some

more recent studies that show that

spironolactone and maybe sglt2

inhibitors do have mortality benefit in

diastolic heart failure but when you're

attending asks you the real answer is

going to be there are no

mortality benefit treatments for

diastolic heart failure and the answer

is going to be we need to treat the

underlying condition and the underlying

condition of diastolic heart failure the

most common one is going to be

uncontrolled hypertension

what is a physical exam maneuver that

has the highest sensitivity for volume

overload this is going to come up on

your board exams and also uh just

something that your attendants might ask

this is going to be looking for jvd in

practicality it's actually very

difficult to see jvd at least in my

experience especially with how obese a

lot of patients are

and so what really we do in practice now

is you'll see a lot of people start

looking at the ivc on a point of care

ultrasound and seeing if they have a

very dilated ivc that's a sign of volume

overload what is the lab test with the

highest sensitivity for chf exacerbation

another board exam question that's going

to be a bnp

and then there are bnp cutoffs that can

essentially rule out if somebody's

having a chf exacerbation and usually if

the bnp is less than 100 they're

probably not volume overloaded

significantly enough to be causing chf

exacerbation

and then really common pimp question

that i just came across so often during

my third year medical school rotation

but what is a reason that bnp may be

falsely low in obese patients that's

going to be because adipocytes degrade

bnp and so your obese patients have a

lot of adipocytes and so they're going

to degrade it and it may be falsely low

what is the goal potassium and magnesium

in patients that are being diurese

that's going to be a potassium greater

than four and a magnesium greater than

two and so this is typically something

that you will be doing in your heart

failure patients uh we'll be replacing

the potassium and magnesium a lot and

the easy way to remember this is that

for every 10 ml equivalents that you

give you are going to raise their serum

potassium by 0.1 so for example if

somebody's potassium is 3.5 and you gave

them 40 ml equivalents of potassium you

would expect their repeat potassium to

go up to 3.9 for magnesium it's for

every 1 gram you're going to go up by

0.1 so if their magnesium is 1.7 then

you can give them 3 grams and that

should raise them up to 2. this basic

conversion is something very useful for

you to know because it comes up very

frequently and then how much lasix

should you give for a chf exacerbation

that's going to be 2 to 2.5 times the

home dose and this is based off the dose

trial and typically what we do is say

that somebody is on 20 milligrams po

lasix daily at home then what we

normally do is we just kind of convert

it 20 milligrams iv lasix because iv

lasix compared to oral lasix is already

kind of like a doubling of the dose and

then finally very very common pimp

question is how long does lasix last and

that's going to be six hours so lasix

lasts six hours that's basically why

it's called lasix now let's do a quick

overview of diabetes so what is the goal

glucose range while hospitalized that's

going to be 140 to 180 milligrams per

deciliter for the nice sugar trial and

this is because when we do a tighter

control in the hospital we increase the

rate of hypoglycemic events so usually

we have a more lenient goal while

patients are hospitalized and then what

outpatient diabetes medications should

you continue while inpatient the answer

to this is usually none except insulin

and the reason is there are a few side

effects of oral diabetes medications

that people are worried about when

patients are hospitalized so what are

people worried about when using

metformin in patients with renal

impairment that's going to be lactic

acidosis now studies aren't very good

for this but it's just a theoretical

fear that a lot of people have

and then why do we hold most outpatient

oral medications on admission so fear of

hypoglycemia if you're giving

sulfonylureas or

anything that kind of is like an insulin

secretog

pancreatic issues with glp1 and dpp4

inhibitors eu glycemic dka is a feared

complication of sglt2 inhibitors and

then heart failure with pioglitazones

which i don't see very commonly uh but

these are some of the reasons that we're

a little bit more hesitant to give oral

medications while they're admitted i

remember as a medical student i never

knew why we were holding all their

outpatient medications so this is the

reason

now what is a newer medication that has

mortality benefit and heart failure with

reduced ef we kind of went through this

already but this is going to be the

sglt2 inhibitors so this is a drug class

that is really really gaining a lot of

favor in diabetic patients what is the

goal a1c in most adults this is another

important question to know but usually

we're just going to target an a1c less

than seven percent and if they're

elderly we're gonna aim for less than

eight percent you know diabetes is

officially diagnosed when your a1c is

greater than 6.5 percent how come we

don't aim for less than six point five

percent well there were some trials that

showed that strict a1c goals less than

six percent was not better than a

lenient goal of less than seven to eight

percent and that was the accord trial

and so that's why we don't try to really

strictly control people's blood sugars

because that increases the rates of

hypoglycemic events and worsens outcomes

does good control of blood glucose

reduce macrovascular complications for

example stroke heart attack things like

that the answer to that is actually no

so even if somebody's a1c is 10 you get

it all the way down to 7

they are still going to have an elevated

risk of stroke and heart attack what it

does uh reduce is microvascular

complications such as peripheral

neuropathy retinopathy and also

nephropathy so treatment of dka revolves

around a few key treatments and that's

going to be fluids very aggressive fluid

hydration because these people are going

to be very volume depleted insulin and

potassium because a lot of times their

whole body potassium depleted as well

and then what are some findings in the

urine and serum of

dka patients that can help diagnose that

they're in a dka episode that's going to

be urine ketones so that's we're going

to look for on urinalysis and then serum

beta-hydroxybutyrate

what value do we trend while treating

patients with dka so we're going to be

looking at their basic metabolic panel

and what we're looking at is we're

looking at their anion gap and we're

waiting for that to close so basically

if you remember your bmp you have your

sodium so let's say they're 135 and you

have potassium say they're four and

chloride 110 and say their bicarb is 10

and their creatinine and bun is 50

and 2 and their glucose is 400 okay so

the way to calculate the anion gap is

gonna be the sodium minus the chloride

minus the bicarb okay so in this case

it's going to be 135 minus 110 minus 10

equals 15. so this person does have an

elevated anion gap usually our anion gap

that we're looking for is an anion gap

less than 12 is normal okay and so we

continue giving insulin and fluids until

we close that anion gap and make sure

that it's less than 12. now let's talk

about endocarditis so what criteria do

we use to diagnose endocarditis very

common pim question this is going to be

the duke criteria and the duke criteria

is listed as here i'm not going to go

through them too much

but some of the things that we see with

endocarditis are immunologic phenomena

and vascular phenomena and i think a lot

of times attendings love to pimp on the

physical exam findings of endocarditis

so immunologic phenomena are include

things like roth spots in your eyes it's

basically these little hemorrhage and

white spots in your eyes and then what's

called osler's nodes on your hands and

the vascular phenomena include splinter

hemorrhages and janeway lesions and the

way to differentiate another common pim

question janeway lesions from oslo's

nodes is that ozer's nodes hurt and

they're painful whereas janeway

and so you can remember that as ousler's

nodes and then janeway lesions are not

painful why do we have to keep repeating

blood cultures for gram-positive

bacteremia so the reason the answer to

that is that gram-positive organisms are

typically a little bit more stickier and

they're harder to clear from the body

than gram negative so if you have a gram

negative e coli bacteremia for example

you can usually just give antibiotics

and you don't necessarily need to check

a repeat blood culture to make sure it's

cleared from the body but if it's staph

aureus or strep or staph epidermidis

then you need to make sure that the

blood cultures have cleared before you

say somebody's been treated

and then now let's move on to gi bleed

so what is the first vital sign to

change in acute gi bleed this is an

important question it's going to be the

heart rate not the blood pressure which

a lot of medical students will get wrong

and then all patients with gi bleed need

two what we went over this earlier but

that's two large bore ivs and what size

defines a large bore iv that's going to

be 18 gauge or larger and so basically

you have like 22 gauge 20 gauge 18 gauge

16 14. so the lower you go the larger

the ivs are getting uh whereas the

higher you go the smaller okay so you

need two 18 gauge or larger ivs and then

can you give rapid fluid resuscitation

through a central line another common

pimp question to medical students the

answer is usually no so if you remember

the law of laplace or whatever the

resistance equation was when you have a

very long catheter you're going to have

huge amounts of resistance and so these

central lines is usually you know going

in an internal jugular vein or going

through a picc line a peripherally

inserted central line and they are very

very long catheters that go all the way

down to the heart and so there's a ton

of resistance and so you actually can't

give huge amounts of fluid rapidly

through those just because of how much

resistance there is now what is the

cutoff point for upper and lower gi

bleed very important question and this

is going to be the ligament of trites

and so anything above the ligament of

trites is an upper gi bleed anything

below the ligament of trites is a lower

gi bleed what are presenting symptoms of

an upper gi bleed this is going to be

melano hematemesis and coffee ground

emesis and then symptoms of a lower gi

bleed is going to be usually hematokesia

and the big differentiating thing that i

want you to know is that if you see a

patient with melanoma that suggests

upper gi bleed and if you see

hematokesia blight bright red blood per

rectum that suggests lower gi bleed very

important for you to know as a medical

student next question does

diverticulosis or diverticulitis bleed

the answer to that is diverticulosis

bleeds whereas diverticulitis hurts so

diverticulosis is again that out

pouching in the colon what it does is it

kind of erodes the area where the

superficial blood vessels are and so

it's prone to bleeding diverticulitis is

kind of when it gets inflamed and

infected and that really hurts but

usually it's not associated with

bleeding so diverticulosis is the one

that bleeds treatment approaches to an

active lower gi bleed this is a pimp

question that i got wrong so i just

threw it in here but you can either do

colonoscopy with banding so you're gonna

clip off those areas that are bleeding

or you can do a ct angiogram look at the

blood vessels and see where the blood is

extravazating from and you can do an ir

embolization to stop that bleeding blood

vessel now what is the transfusion goal

for hemoglobin very important question

that you're going to get asked and this

is going to be

if patients hemoglobin is less than

seven then that's usually our threshold

for

transfusing

transfusion goal for platelets is going

to be usually if the platelets are less

than 10 000 then we are going to

transfuse if they're actively bleeding

then we usually transfuse if it's less

than 20 000 and if they're pre-op you

know getting ready for a procedure

sometimes we have a higher goal of 50

000 and the reason that we transfuse

once the platelets are less than 10 000

is usually that has a risk of

intracranial hemorrhage spontaneous

brain bleed so that's why we transfuse

if it's that low

what is a lab value that you can check

on the basic metabolic panel that can be

elevated in a slow gi bleed that's going

to be the bun

there's a lot of nitrogen in blood and

your blood um gets digested in the gi

tract so it can really elevate your bun

that's something you can look out for

now let's talk about sepsis so what is

the cutoff temperature for defining

fever that's going to be 100.4 degrees

fahrenheit or 38 degrees celsius what

are the sirs criteria you should

definitely know this it's going to be

temperature heart rate respiratory rate

and white blood cell count and

interestingly there's a new set of

criteria that helps predict mortality

from sepsis and it's supposed to be more

accurate than the sirs criteria and

that's going to be q sofa so this is

something that you might get asked about

the criteria for this includes altered

mental status respiratory rate and blood

pressure and then what was the old

definition of sepsis severe sepsis and

septic shock

definitely a lot of old school tendings

are going to be asking something like

this so

sepsis is two plus of sirs plus a

suspected infection and then if you have

signs of organ damage then you call it

severe sepsis and then finally septic

shock what differentiates septic shock

from uh severe sepsis is that you have

hypotension that is unresponsive to

fluids okay so this is described here

now the thing is with the new sepsis

guidelines we've kind of removed the

severe sepsis category so now we just

have sepsis and septic shock so that's

something that's a little bit new now

next question when you're drawing blood

cultures how many sets of blood cultures

should you get we usually get two sets

of blood cultures because sometimes you

can get false positives or contaminants

so we get two just to make sure that we

have an accurate blood culture and then

how much fluid do you typically give for

sepsis that's going to be 30ccs per

kilogram this is per the surviving

sepsis guidelines but this is now

outdated but if you're attending ask

this then you should definitely know

that usually our goal is giving 30ccs

per kilogram now it's a little bit more

individualized but the answer to your

attend attendance question is gonna be

30 ccs per kilogram and then what are

the four key components of treating

sepsis that's going to be fluids

antibiotics source control and pressers

so definitely need to get those fluids

and antibiotics started asap and then

source control is like if somebody has

an abscess and you're just giving

antibiotics you're not actually getting

source control on that infection you

really need to target that area that's

infected and drain that abscess in order

to really treat it because if you just

give antibiotics it's not going to be

sufficient now let's talk about

pancreatitis so how do you diagnose

pancreatitis very important set of

questions so you need at least two out

of three of the following findings you

need typical symptoms so that's going to

be epigrastric abdominal pain that

radiates to the back you need a lipase

level that's greater than three times

the upper limit of normal and you need

radiographic evidence for example a ct

scan showing inflammation around the

pancreas so you need two of those three

criteria and then you can diagnose

pancreatitis and the most important

aspects of treating pancreatitis there's

two main treatments that we're going to

be using that's going to be fluids and

pain control what are the two most

common causes of pancreatitis the answer

to that is going to be gallstones and

alcohol very important question for you

to know and a common mnemonic for other

causes of pancreatitis is going to be

the get smashed mnemonic i don't

actually know the whole mnemonic off the

top of my head but one common pimp

question that you're going to ask is

what is a very weird unique or odd cause

of pancreatitis and the answer to that

is going to be scorpion bites is a very

rare but interesting cause of

pancreatitis

should patients with pancreatitis be

made npo the answer is no you should

advance their diet as tolerated the

prevailing thought in the past was you

should allow bowel rest to make sure

you're not secreting you know pancreatic

enzymes and causing more inflammation

but the studies have shown that actually

advancing diet is tolerated has had

improved outcomes compared to making

people on full bowel rest and then are

antibiotics indicated for pancreatitis

and the answer to that is generally not

and what are scoring systems for

predicting mortality from pancreatitis

that's going to be the bisap and the

ransons criteria so biceps stands for

bun impaired mental status sirs criteria

age and pleural effusion and then why

might hemoglobin and bun be elevated in

patients with pancreatitis so what

happens is they're releasing all these

digestive enzymes and these digestive

enzymes are super irritating and they

cause blood vessels to become very leaky

and so what happens is you get profound

hypovolemia from capillary leak

basically all their fluid is just like

third space and so it concentrates all

the things that are in your blood like

your hemoglobin and your bun now why

might calcium be low this is a pimp

question that i got and this is because

those pancreatic enzymes actually bind

to calcium in a process known as

saponification now let's talk about

pneumonia there's two main types of

pneumonia that you should know because

our treatments kind of vary for these

and that's going to be community

acquired pneumonia and hospital acquired

pneumonia so what are some scoring

systems that determine if a patient

needs to be admitted that's going to be

the curb 65 and the pneumonia severity

index and what our typical antibiotics

that we give for community acquired

pneumonia while patients are admitted

that's gonna be ceftriaxone and

azithromycin that's the most typical

regimen that you're gonna see and then

what if a patient has a risk factor for

mrsa what are you gonna add you're gonna

add vancomycin and if they have a risk

factor for pseudomonas you're going to

use cefepime or pipracillin taseobactam

also known as zosin instead of

ceftriaxone because it has

anti-pseudomonal coverage and then if

you expect esbl so extended spectrum

beta lactamase now we have to upgrade

even higher that's going to be using

carbopenes which have activity against

espl's there is only one carbopenem that

does not cover pseudomonas and that's

going to be ertapenum uh the advantage

of erdopenum is that it's once daily

dosing so ertopenum is kind of different

from all of the other carbopenems and

then what is the definition of hospital

acquired pneumonia a very important

question that's going to be any

pneumonia that develops greater than 48

hours after admission and usually when

somebody develops hospital acquired

pneumonia we automatically start them on

pseudomonal coverage because they have

that's basically a risk factor for

pseudomonas so they'll usually start on

cefepime or zosin based on your

institution and then plus or minus

vancomycin depending on the mrsa rates

at your hospital as well and then do you

need anaerobic coverage for aspiration

pneumonia this is something that you

know we have a lot of anaerobic flora in

our oral flora and so when you aspirate

uh you know people ask oh maybe we need

to add metronidazole to cover anaerobes

the answer for that is no based on the

2019 idsa guidelines the only reasons

you would add metronidazole would be if

there's an abscess or an empiema is

suspected because if you think about it

the lungs are an aerobic environment so

anaerobes are not going to survive

anyways only if there is a walled off

abscess or a focal fluid conduction can

anaerobes actually be able to survive

now let's talk about uti so what are ua

findings that are suggestive of uti

that's going to be leukocyte esterase

nitrites white blood cells and bacteria

so leukocyte esterase is basically an

enzyme that white blood cells produce so

that tells you that white blood cells

are active right now and then nitrites

are kind of like this enzyme that

bacteria release so that's another sign

that you might have a urinary tract

infection and then one other thing is

that if you see squamous cells on your

ua that indicates that the sample is

potentially contaminated it wasn't a

very good clean catch so sometimes it

might not be as accurate now should

asymptomatic

bacteria urea be treated so you see a

patient e coli is greater than a hundred

thousand colony forming units but they

have no dyseria no suprapubic tenderness

no symptoms at all the answer is no the

only time we really treat it is uh

pregnant patients because they have

worse outcomes if you treat if you don't

treat their bacteria urea

and then uh most common organism causing

a uti this is a good pimp question for

medical students and it's going to be e

coli and then other gram negatives like

klebsiella and serratia and then what is

a typical antibiotic that we use for

treating uti while inpatient that's

going to be ceftriaxone gives a lot of

that good gram negative coverage and

then if there's a risk factor for

pseudomonas kind of like with pneumonia

we're going to upgrade to cefepime or

zosin for the anti-pseudomonal coverage

and then how do you define complicated

uti versus simple cystitis so

complicated uti is basically saying that

there's

signs of infection past the bladder

whereas simple cystitis is combined only

to the bladder so whereas with simple

cystitis you may have some suprapubic

tenderness you may have some dysuria or

urinary frequency complicated uti is

going to be defined when you have a

fever

chills flank pain which and cva

tenderness which would be concerning for

extension up to the kidneys like

pyelonephritis

and common antibiotics that we use to

treat simple cystitis as an outpatient

that's going to be nitrofurantoen and

trimethopyrium sulfur methoxazole or

bactrim and then common antibiotics used

to treat a complicated uti as an

outpatient that's going to be

something like a fluoroquinolone and so

the fluoroquinolones are kind of like

our big guns as the outpatient regimen

and a fluoroquinolone that does not

provide good uti coverage is going to be

moxifloxes in the ones that we would use

instead is going to be ciprofloxacin and

levofloxacin both of which have good

urinary

penetration now let's talk about

hyponatremia the internist favorite talk

but people think that you know this is a

lot of like mental masturbation and

we're not really you know we're just

talking about what the etiology of

hyponatremia is and it's really useless

but actually it's very very important to

know what the etiology of hyponatremia

is because the treatment's completely

differ based on what the etiology is so

that's why it's actually very important

to know hyponatremia so first of all uh

what is the mnemonic for remembering the

danger of overcorrecting hypo or

hypernatremia that is going to be low to

high ponds will die or osmotic

demyelination syndrome and high to low

brains will blow cerebral edema so for

example sodium was 110 and then in 24

hours you corrected it to 135 then

you're worried about osmotic

demyelination and then in this scenario

uh you know sodium was 160 and you

corrected it to 140 all of a sudden then

you're worried about cerebral edema very

useful mnemonic to know

how do you differentiate acute versus

chronic hyponatremia that's going to be

less than 48 hours is acute and greater

than 48 hours is chronic and the reason

that's important is because for acute

hyponatremia less than 48 hours you can

correct it right away and not have to

worry about osmotic demyelination now

what is the goal correction rate for

chronic hyponatremia so we want to be a

little bit more gentle to prevent

osmotic demyelination that's going to be

about six to eight mil equivalents per

day and then what is the first thing to

assess after seeing a patient has

hyponatremia so this is a very common uh

question that you might get asked it's

also going to be on your board exams and

also you'll see it in all these

algorithms for diagnosing the etiology

of hyponatremia so if you see a patient

comes in sodium is 120 what do you want

to look at first the first thing you

look at is the osmolality all right so

there's three possibilities you can have

a hypertonic osmolality you can have

isotonic and then you can have hypotonic

the reason this is important is because

the differential completely differs so

the most common cause of hypertonic

hyponatremia you know say your

osmolality is like greater than 295 the

most common cause of that is going to be

hyperglycemia and then the most common

cause of isotonic so if your osmolarity

is like 285 to 295 it's going to be

pseudohyponatremia and what

pseudohyponatremia is is basically it's

a lab error and usually due to too many

proteins

or too many lipids or triglycerides and

then finally if you have hypotonic which

is less than 285

we'll go into that in a little bit so a

patient presents with glucose 500 and

sodium of 126. this is another

important question but we have to

correct their sodium for their degree of

hyperglycemia so what is their true

sodium so the way to do this is that for

every

100 glucose above 100 add 2

to the sodium

so this person has 4 100s

above 100 right so you do 4 times 2

equals 8. so you do 126 plus 8 equals

134 so that's what their sodium is going

to be after doing correction for

hypoglycemia very common thing that you

may have to do while you're in the

hospital okay so next question is the

next thing to assess after determining a

patient has hypotonic hyponatremia this

is the most common cause of hyponatremia

that we see and now we want to look at

their volume status okay and this is

super super important because it totally

dictates our treatment so i'm just going

to do a very superficial discussion but

if your patient has hypovolemic

hyponatremia our treatment is usually

going to be fluids if they have

euvolemic hyponatremia it's going to be

usually fluid restriction the most

common cause of this is going to be

siadh and then finally if they have

hypovolemic hyponatremia our treatment

is going to be diuresis so this is

really the crux of why it's so important

to know what the etiology of

hyponatremia is because our treatments

vary so much between each of these

different etiologies one we give fluids

one we hold fluids one we try and get

rid of fluids right so when people come

into the ed and people just blindly give

fluids for hyponatremia a lot of times

they cause worsening of their

hyponatremia so you really need to think

about what their actual ideology of

hyponatremia is that's why we spend so

much time thinking about why they have

hyponatremia finally what are the most

common causes of hypovolemic

hyponatremia that's going to be chf

cirrhosis and nephrotic syndrome all

these different

conditions that can cause whole body

volume overload and cause low sodium

levels now these are the two algorithms

that i really like this one is from

american family physicians i just every

time i want to look it up i just go to

google images and i just type afp

hyponatremia algorithm and so this

really shows you first we look at the

osmolality we see if it's hypertonic

then it's probably hyperglycemia if it's

normal then it's probably

pseudohyponatremia and if it's low then

we go down and we check at their volume

status hypovolemic we usually give

fluids euvolemic we usually do fluid

restriction and hypervolemic we usually

do diuresis

another super helpful one that i've also

liked and kind of comes at it from a

different perspective is the clinical

problem solvers

algorithm for hyponatremia as well

okay let's talk about hyperkalemia so

what is the first test that you want to

get if the potassium is high that's

going to be an ekg the first ekg finding

of hyperkalemia is going to be peaked t

waves and the next ekg finding of

hyperkalemia is going to be widened or

prolonged qrs and then finally if you

continue to not treat their hyperkalemia

what's going to happen they're going to

develop a sine wave and then they're

going to progress into ventricular

fibrillation asystole or pulseless

electrical activity they're going to die

so that's why we check an ekg because we

want to see how much these high

potassium levels are actually

impacting their

cardiac conduction now what is a

treatment that we give to stabilize the

cardiac membrane so if you see any ekg

changes then we immediately give this

treatment it's going to be calcium

gluconate and then finally we have some

temporizing measures that are useful

to lower the potassium levels

temporarily and that's going to be

insulin plus d50 sodium bicarbonate and

albuterol so how this works insulin

again works through the sodium and

potassium atpase so you give them both

insulin and d50 to make sure they don't

get hypoglycemic but the insulin drives

potassium into cells the same thing

happens with sodium bicarbonate so if

you're making their ph of their blood

more alkaline what happens is that h

plus ions in their cells will go out

into the blood to try and make it more

acidic again and then that's they need

to be exchanged for another positive ion

so the potassium will go back into their

cells and then albuterol also works with

the sodium potassium atpase and causes

shift of potassium into cells but again

these are only temporary measures that

only last for about one to four hours so

instead we need to do treatments that

actually permanently get rid of the

potassium and that's going to be things

like lasix because you're going to be

peeing out the potassium uh local or

caxallate which are basically potassium

binders that go through the gi tract and

then finally dialysis you know if

somebody's got very high potassium

levels 7.5 got lots of ekg changes and

you're not going to be able to temporize

them then they just need emergent

dialysis so what is the framework for

different causes of elevated potassium

this is going to be electrolyte shifts

excess intake or release

usually this is going to be you know

rhabdo you know cells are lysing tumor

lysis syndrome cells have a ton of

potassium in them so it can cause

hyperkalemia and then poor excretion

this is usually going to be renal

failure kidney failure not able to pee

out that potassium but also constipation

can cause hyperkalemia as well

now let's talk about acute kidney injury

and dialysis very important topics to

know because so many of our patients

come in with acute kidney injury so what

is the definition of an aki based on the

creatinine level so this is an important

question to know aki is defined by a

creatinine greater than 0.3 from their

normal baseline or greater than 50

percent of their baseline so if their

cratinine is normally 1 and it comes in

at 1.2 they're not quite at an aki level

yet but if it's 1.3 then you would

define that as an aki and then how long

should creatine be elevated before you

call it chronic kidney disease so now

it's progression of their kidney disease

that takes three months so if now he's

been at 1.3 and it's just for the next

three months it just stays at 1.3 it

never goes down now that's his new

baseline and we call it ckd

there are three categories of aki it's a

nice framework for determining what the

cause of their aki is and that's going

to be pre-renal intra-renal and

post-renal very important question that

you're very likely to get pimped on and

then what is a lab test that you can use

to help differentiate pre-renal versus

intra-renal ek aki that's going to be a

phena fractional excretion of sodium or

feuria if a patient is on a diuretic

honestly the studies regarding these are

actually not that useful but this is

something you can definitely get asked

about on your internal medicine rotation

and then what are indications for

dialysis huge huge question that you're

going to get asked all the time that's

going to be a e i o u basically all the

letters of the alphabet so a is for

acidosis if their ph is 6.9 you need to

dialyze them e is for electrolytes

usually this is hyperkalemia if they're

potassium 7.9 you're going to ekg

changes like we mentioned in the last

slide then you need to dialyze i is for

ingestion of talk or intoxicants any

like toxic things

o is for overload if they're severely

volume overloaded they're not making

urine then you need to dialyze and get

that volume off and then u is for uremia

so if their bun is like 100 plus and

they're uremic they're encephalopathic

that is an indication for dialysis

what is the type of imaging we're

concerned about getting in patients with

aki or ckd that's going to be any

imaging that uses contrast because there

is a concern that contrast can cause aki

by causing vasoconstriction and what

happens is a patient goes and gets a ct

abdomen and pelvis with contrast and

then we see an aki a few days later so

the typical timing for contrast induced

nephropathy is really going to be two to

three days

and how much of a creatinine rise is

expected after starting an ace inhibitor

that's going to be up to a 30 percent

increase in their creatinine and then is

a creatinine increase from one to two or

three to four more significant this is

an important question you might get

asked so

i'm gonna just show you uh how one to

two is a lot more significant and a lot

more worrisome compared to three to four

or even three to five you know something

like that i'm not as worried as you know

one to two so this is a graph of your

gfr compared to your creatinine level so

say your creatinine is one so if we

trace it all the way over here then your

gfr is like 100. now if you go from one

to two now all of a sudden you've

dropped your gfr from 100 to 20. if you

go from three to four you've basically

only gone from 17 to like 15. so you can

see how changes in creatinine at lower

levels has a much bigger impact on your

gfr than if somebody already has very

high creatinine

what is the most important marker of

kidney function so we talk about

creatinine all the time but truly the

most important marker of kidney function

is going to be looking at the patient's

urine output because that's really going

to tell us how the kidneys are

functioning now let's go do a hodgepodge

of different questions antihypertensives

dvtpe and aortic stenosis so what is the

goal blood pressure for outpatients this

is really nice to know the goal is

usually going to be less than 130 over

80. this is per the sprint trial

which showed that less than 120 over 80

was good but then there's a chord trial

which showed that less than 140 over 90

was good so now they kind of just took

the middle of that and now it's like

less than 130 over 80. and then if

they're more elderly you can be a little

bit more lenient because we want to

prevent episodes of hypotension

what are the three first-line

anti-hypertensives very important to

know ace inhibitors calcium channel

blockers and thiazides per the all hat

trial and then importantly not beta

blockers okay beta blockers are not

considered a first line antihypertensive

they're actually actually pretty bad at

controlling blood pressure and what is a

triad of risk factors for developing dvt

slash pe that's going to be called

vercause triad so that's going to be

hypercoagulable state

venous stasis and endothelial injury and

then what is a score that we can use to

evaluate the likelihood of pe these are

important scores to know about it's

gonna be the wells score and the pe rule

out criteria and so pe rule criteria if

they score zero on this you can

officially rule them out for uh pe if

not then you can use the well score to

risk stratify are they a low risk of pe

or a high risk of pe and then next we

can get a lab test that can help us

assess the risk of p e and that's going

to be a d dimer so d dimer is basically

a byproduct of clot degradation so if

there's a clot you'll see an elevated

d-dimer which could be

suggestive of a pe or dvt

but one important question that people

always always always ask medical

students is is d-dimer useful in

patients with a high well score so these

are patients where you have high

suspicion

of pe okay and is d dimer useful the

answer is no d dimer is only useful in

lower scores less than four in order to

rule out the need for a ct scan to look

for a pe and so this makes sense because

if you have high suspicion for a pe and

then you get the d dimer and it's

negative you still have a high suspicion

of pe so you're going to progress to

that you're going to go to that ct scan

anyways the only situation in which it's

useful is when you have a low well score

that means you have a low suspicion for

p e and then you get a d dimer which is

negative which confirms that you have a

low suspicion okay so that's you only

get d dimer if it's a low well score

part of the well score is unilateral leg

swelling and that is defined by a

greater than three centimeter

circumference compared to the other leg

and then what is the medication we use

to prevent dvts and hospitalized

patients that's going to be lovinox or

heparin if patients have renal

impairment and then there's a name of

mechanical methods of dvt prophylaxis so

we like strap these things on patients

legs and basically massage their legs

and squeeze to try and promote blood

flow and that's going to be scd or ipc

sequential compression device or

intermatic pneumatic compression device

um and the evidence for these is not

super great but it's better than nothing

because sometimes we can't put patients

on heparin or lovenox or any blood

thinner next what are the three cardinal

symptoms of aortic stenosis a very

important question to know

but this is going to be angina syncope

and heart failure and then what is the

mortality rate of aortic stenosis after

you develop the above symptoms so angina

has a five-year 50 mortality syncope has

a three-year 50 mortality and the

development of chf has a two-year 50

mortality and then does the loudness of

the murmur correlate with the severity

these are all pimp questions that i got

asked when i was in medical school but

the answer is no so if you hear a very

very loud crescendo decrescendo murmur

that does not necessarily tell you how

severe the aortic stenosis is

instead there are other physical exam

characteristics that are suggestive of

more severe as and that's going to be a

late peaking murmur a diminished s2 and

pulses parvis at tardis

now let's talk about general healthcare

maintenance last slide almost there guys

so influenza vaccination is going to be

yearly pneumonia vaccination is going to

be for all adults greater than 65 plus

but if they have a lot of these comorbid

conditions

then you usually do 21 plus so if

there's smoker heart failure diabetes

alcoholism and there's a whole slew of

other conditions and also

different vaccinations that we use

different timings of the vaccinations

but in general all adults over 65 plus

or 21 plus if they have different

comorbid conditions tdap vaccination is

going to be every 10 years shingles

vaccination is going to be at age 50

plus

colon cancer screening is going to be a

colonoscopy starting at the age of 50

all the way up to 75 and you need a

routine one every 10 years the main

exception for this is if you have ibd

then you get your first colonoscopy

after eight years after diagnosis and

then every one to two years after that

and then if you have a family history of

colon cancer then you do 10 years before

your relative got colon cancer or age 40

whatever comes earlier so for example if

your relative got diagnosed with colon

cancer at age 44 then you would have to

get your first colonoscopy at age 34. if

your relative got colon cancer at age 53

then you would get your first

colonoscopy at age 40 because age 40 is

earlier than 10 years less than 53 which

is 43.

okay osteoporosis screening is

recommended as a one-time dexa

after the age of 65 for all females and

then breast cancer screening is going to

be from age 50 to 74 with a mammogram

every two years and a risk benefit

discussion if they're higher risk you

can start screening at the age 40 as

well cervical cancer screening is going

to be ages 21 to 64 with a pap smear

every three years or a pap plus hpv test

every five years lung cancer screening

is very important one to know because

you might get asked about this

but this is from ages 55 to 80 with a 30

pack year smoking history and they're

currently smoking or quit in the last 15

years so very important that we only get

a ct scan to screen for lung cancer if

they have this 30 pack year smoking

history and if they're a recent or

currently smoking person and then

abdominal aortic aneurysm screening is

going to be any man who is a smoker

between age 65 to 75 and then diabetes

screening usually is going to be at age

45 plus but any patients with comorbid

conditions like hypertension obesity

other risk factors

and asians usually get screened a little

bit earlier too

then those are indications to screen

earlier but otherwise age 45 plus

everybody should get an a1c prostate

cancer screening

recently the uspstf had recommended

against prostate cancer screening

routinely but now they've changed it

back to a risk benefit discussion so

this is uh between men age 55 to 69 and

keep in mind that african american men

are at higher risk so i highly recommend

when you're doing your outpatient family

medicine or internal medicine rotation

you really need to review the uspstf

guidelines which gave all the guidelines

to routine screenings that we do as

outpatients all right and that is it for

my guide to internal medicine for third

year medical students if you made it

this far congratulations it was a long

one and i hope there was a ton of high

yield information in this present

presentation and i'm sure that this is

going to help you get a lot of pimp

questions right on your uh rotation

because i know these are all the

questions that i had gotten asked and i

thought were high yields and important

for you to know if you have any

questions or comments definitely leave

them down in the comment section down

below and i will 100 respond to them and

answer any questions that you guys have

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