Deck 1 Flashcards
What is a mnemonic for the causes of clubbing?
CLUBBING ABCDEF
Cyanotic heart disease Lung disease UC + Crohn's Biliary Cirrhosis Birth defects Infective Endocarditis Neoplasm GI malabsorption syndrome (celiac)
Abscess Bronchiectasis Cystic Fibrosis DONT SAY COPD Empyema Fibrosis
DDx lower GI bleeding
Colorectal cancer or polyps Diverticulosis Angiodysplasia Anorectal disease Enterocolitis Brisk bleeding from upper GI Rectal trauma
**pay particular attention to the hemodynamics lily unstable patient
DDx upper GI bleed
- Ulcerative or erosive processes–> PUD, esophagitis, gastritis
- Portal HTN
- Trauma (I.e Mallory Weiss tear)
- Tumours
DDx hemoptysis
- Airway disease–> inflammatory (bronchiectasis, bronchitis); neoplasms (bronchogenic carcinoma); other (foreign body, trauma)
- Pulmonary parenchymal disease–> infectious (TB, necrotizing pneumonia); inflammatory/immune (vasculitis); other (coagulopathy)
- Cardiac/vascular–> PE with infarction; elevated capillary pressure (mitral stenosis, LV failure); AV malformation
DDx abdominal distension
- Ascites–> low serum to ascites albumin ratio = exudative (peritoneal carcinomatosis); high serum to ascites albumin ratio = transudative (portal HTN)
- Bowel dilation–> mechanical obstruction (adhesions, volvulus); Paralytic (toxic megacolon, neuropathy)
- Other–> abdominal mass, IBS, organomegaly (hepatomegaly), pelvic mass (I.e ovarian cancer or others)
DDx hematuria
- Glomerular disease–> SLE, hemolytic uremic syndrome, vasculitis
- Post renal–> stones, bladder tumour, BPH, cystitis
- Haematological–> coagulopathy, sickle hemoglobinopathy
DDx cardiac arrest
CAD
Cardiac conduction abnormalities
Myocardial abnormalities
Non cardiac (I.e PE)
DDx chest pain
- Cardiac
- -A. Ischemic –> ACS, stable angina pectoris
- -B. Non-ischemic–> aortic aneurysm, pericarditis - Pulmonary or mediastinal
- -PE or pulmonary infarct
- -Pleuritis
- -Pneumothorax
- -Malignancy - GI
- -esophageal spasm or esophagitis
- -PUD
- -Mallory Weiss syndrome
- -biliary disease or pancreatitis - Anxiety disorders
- Chest wall pain (I.e costochondritis)
DDx dyspnea
- Cardiac
- myocardial dysfunction (I.e ischemic cardiomyopathy)
- valvular heart disease
- pericardial disease (I.e tamponade)
- increased cardiac output (I.e anemia)
- arrhythmia - Pulmonary
- upper airway (foreign body, anaphylaxis)
- chest wall and pleura (pleural effusion)
- lower airway (asthma, COPD)
- alveolar (pneumonia) - Central (metabolic acidosis, anxiety)
DDx lymphadenopathy
- Localized
- Reactive (I.e tonsillitis)
- Neoplasticism (metastatic cancer) - Diffuse
- infectious (I.e viral)
- inflammatory (I.e sarcoidosis)
- neoplastic (I.e lymphoma)
DDx pleural effusion
- Transudative–> I.e CHF, nephrotic syndrome, cirrhosis
- Exudative–>
- A. Infectious (parapneumonic, empyema, TB)
- B. Neoplastic (primary, mets, mesothelioma)
- C. Cardiac/vascular (I.e PE, collagen vascular disease)
- D. GI (I.e ruptured esophagus, pancreatitis, chylothorax)
DDx hyperkalemia
- Increased intake (usually associated with low excretion)
- Redistribution
- A. Decreased entry into cells–> I.e insulin deficiency, beta 2 blockade
- B. Increased exit from cells–> I.e metabolic acidosis, rhabdomyolysis - Reduced urinary excretion
- A. Decreased glomerular filtration rate–>I.e acute or chronic kidney disease
- B. Decreased secretion–> I.e aldosterone deficiency, drugs (I.e spironolactone)
* *dont forget to order and ECG to look for changes! (“T waves you wouldn’t want to sit on”)
DDx hypokalemia
- Decreased intake (I.e anorexia nervosa)
- Redistribution (I.e alkalemia, insulin, beta 2 adrenergic stimulating drugs)
- Increased losses, either renal or GI (I.e vomiting/diarrhea)
DDx weight loss
- Decreased nutritional intake–> psychiatric disease (anorexia, bulimia, depression), medical disease (chronic illness, esophageal cancer), illicit drugs or meds (alcohol, opiates, cocaine, amphetamines, anti cancer drugs)
- Increased energy expenditure–> hormonal (I.e hyperthyroid), chronic illness (COPD, HF), malignancy, infection, excessive physical activity (I.e runners)
- Caloric loss–> malabsorption (I.e diarrhea), diabetes
Define heart failure
Occurs when the hearts function as a pump is inadequate to maintain adequate perfusion, or the heart is only able to do so at HIGHER FILLING PRESSURES
SYNDROME not a diagnosis –>must determine underlying etiology
CLINICAL dx, do not need to wait for an echo to diagnose (though an echo can give further info on the underlying pathology behind the clinical presentation of heart failure)
What are the two key questions to ask yourself about HF?
- What type of HF is it
2. What is the etiology
what should you ask on history for an upper GI bleed?
- blood–> hematemesis, coffee ground emesis, melena, hematochezia (if brisk)
- abdominal pain
- hx of gerd
- medications
- EtOH consumption
what to look for specifically on physical exam for an upper GI bleed
- vitals–> tachy? hypotension or HTN?
- signs of anemia
- signs of liver disease
- FOB
investigations for upper GI bleed
CBC and diff chem-7 LFTs and lipase INR, PTT, group and screen urea breath test serology
how would you manage an upper GI bleed?
- keep patient NPO–> send for EGD–> can be either diagnostic only or therapeutic i.e bleeding control with epinephrine/thermal hemostasis, endoclips, hemospray
- pantoloc 80 mg IV bolus then 8mg/hr thereafter
- variceal bleeds require octreotide
- consider iron supplements and fluids–> transfusion if hemoglobin drops and/or symptomatic and/or large bleed
- advise patient of lifestyle changes
- hold offending meds i.e NSAIDs, bisphosphonates, anticoagulants
- if H. Pylori is a factor–> triple therapy: PPI +amoxicillin + clarithromycin // quadruple therapy: PPI + bismuth + tetracycline +metronidazole
DDx for lower GI bleed
Common: diverticulosis--> CT to assess ischemic bowel--> lactate and CT angio infectious--> SECSY bacteria hemorrhoids, fissure
Less common:
brisk UGIB
IBD (UC>CD)
CRC or bleeding polyps
Other: coagulopathy/thrombocytopenia, post surgical bleed
what to ask on history for a LGIB
characterization of blood
abdominal pain
PMHX–cancer, IBD, diverticulosis
medications–anticoagulants, NSAIDs
anemia sx
B symptoms
infection sx
what to look for on physical for LGIB
are they hemodynamically stable?–vitals
signs of anemia
abdominal tenderness/masses
rectal exam
investigations for a LGIB
CBC and diff
chem 7
PTT, INR, group and screen, lactate
liver panel
stool C+S, FOB
colonoscopy, consider and EGD if suspect UGI etiology
consider angiography if suspect ischemic bowel or vasculitis
treatment for LGIB
IV fluids–> transfuse if necessary
hold anti hypertensives and diuretics
consider vitamin K, FFP if needed
DDx of chronic/recurrent abdominal pain
- inflammatory
- PUD
- biliary colic
- IBD
- chronic pancreatitis - neoplastic or vascular
- recurrent bowel obstruction
- mesenteric ischemia
- sicke cell anemia - toxin
- lead poisoning - other
- mittleschmertz
- endometriosis
- porphyria
- IBS
- radiculopathy
- abdominal wall pain syndrome
what should you make sure to rule out in acute upper abdo pain?
make sure you rule out thoracic sources like MI, pneumonia, dissecting aneurysm
DDx for acute inflammatory diarrhea
- bacterial
- shigella
- salmonella
- campylobacter
- yersinia
- E. coli (hemorrhagic)
- C. diff - protozoal
- entamoeba histolytica
- strongyloides - others
- NSAIDs
- IBD
- ischemic
define inflammatory diarrha
when there is damage to the mucosal lining or brush border which leads to passive loss of protein rich fluids and a decreased ability to absorb these lost fluids
**blood only found in inflammatory diarrhea
diarrhea may be perfuse or very small in volume
often associated with abdominal pain and fevers/chills
define non inflammatory diarrhea
no damage to the mucosal lining… N/V may be present
NOT present: fevers, chills, blood in stool, severe abdo pain or tenderness
DDx non inflammatory diarrhea
- bacterial
- S. aureus
- C. perfringens
- B. cereus
- E coli (ETEC and EPEC)
- salmonella enteritidis
- vibrio cholera - protozoal
- giardia - viral
- rotavirus
- norwalk
- CMV - drugs
- antibiotics
- colchicine
- laxatives
- antacids (magnesium)
what should you rule out first when patients present with bloody diarrhea
IBD
DDx chronic diarrhea
- inflammatory
- IBD
- infectious (TB, Cdiff, CMV, HSV)
- ischemic bowel
- radiation colitis
- neoplasia - secretory
- stimulant laxatives
- post ileal resection/cholescystectomy
- bacterial toxins
- vasculitis
- neoplasia
- addison’s disease
- congenital syndromes - steatorrheic
- giardia
- celiac sprue
- chronic pancreatitis
- chronis cholestasis - osmotic
- osmotic laxatives
- lactose intolerance
- chewing gum - functional
- IBS
- constipation (overflow diarrhea)
- anal sphincter dysfunction
DDx nausea/vomiting with abdominal pain and relieved by vomiting
gastric outlet obstruction
small bowel obstruction
GERD (regurg)
DDx nausea/vomiting with abdominal pain and NOT relieved by vomiting
gallbladder disease pancreatitis MI hepatitis infectious gastroenteritis
DDx nausea/vomiting without abdominal pain and associated with headache/dizziness
cerebral tumor
migraine
vestibular disease
increased ICP
DDx nausea/vomiting without abdominal pain and with no other symptoms
drugs uremia pregnancy metabolic (hypercalcemia) gastroparesis (i.e diabetes) ketoacidosis
DDx abdominal distension with FLUID
- with portal HTN
- cirrhosis
- cardiac failure
- hepatic vein thrombosis - with normal portal pressure
- cancer (especially OVARIAN)
- pancreatitis
- TB
DDx abdominal distension with flatulence
functional bowel disease (IBS) fibre lactose intolerance chewing gum (sorbitol, mannitol)
DDx abdominal distension with reduced feces output
constipation
colonic obstruction
dysmotility
DDx abdominal distension–other
pregnancy
obesity
blood
large tumors
what is a mnemonic to remember a DDx for abdo distension
the 6 Fs Fat Feces Fetus Flatus Fluid Fatal growth (large tumors)
DDx for jaundice with high UNconjugated bilirubin
- overproduction
- hemolysis
- ineffective erythropoeisis (i.e in megaloblastic anemias) - decreased hepatic intake
- gilbert’s syndrome
- drugs (i.e rifampin) - decreased conjugation
- drug inhibition
- Crigler-Nair syndromes type I and II
- Gilbert’s syndrome
- neonatal jaundice
DDx for jaundice with CONjugated bilirubin
-common: drugs cirrhosis inflammation (hepatitis of any cause) infiltrative (i.e hemochromatosis) familial disorders (dubin-johnson etc) PBC PSC sepsis post op/TPN
-less common:
1. intraductal obstruction
gallstones
biliary stricture
parasites
malignancy (cholangioca)
sclerosing cholangitis
2. extraductal obstruction
malignancy (i.e pancreatic cancer or lymphoma)
mets in peri portal notes
3. inflammation
foods/substances that aggravate GERD sx
EtOH caffeine tobacco fatty/fried foods chocolate peppermint spicy foods citrus fruits
typical symptoms of GERD
heartburn acid regurd sour regurg water brash sensation of lump in throat (globus sensation) frequent belching
non-esophageal sx are poor predictors of reflux
i.e chronic cough, wheezing, sore throat, hoarseness, dental erosions
indications for gastroscopy in GERD
heartburn with red flags like bleeding and weight loss
persistent reflux sx or prior severe erosive esophagitis after therapeutic trial of 4-8 weeks of PPI 2x daily
history of esophageal stricture with persistent dysphagia
treatment for reflux
PPIs are most effective, relief in 80% of cases –usually need to be continued as maintenance
can use antacids, H2 blockers for on demand relief
diet helps the symptoms not the disease–avoid aggravating foods
the only beneficial lifestyle change is weight loss if obese and elevating the head of the bed at night if having nocturnal symptoms
complications of GERd
esophageal stricture disease
ulcer
bleeding
barretts esophagus/esophageal carcinoma
red flags of dyspepsia that raise suspicion of gastric malignancy
unintended weight loss persistent vomiting progressive dysphagia odynophagia unexplained anemia or iron deficiency hematemesis jaundice palpable abdominal massor lymphadenopathy family history of GI cancer previous gastric surgery
what is Carnetts sign
during exam for dyspepsia—indicates an abdominal wall muscle problem
pain increases during muscle contraction (i.e sit up)
how is gastritis defined
histologically–inflammation of the stomach mucosa
define PUD
focal defects in the mucosa that penetrate the muscularis mucosa of the stomach or duodenum resulting in scarring
etiology of PUD
h pylori infection NSAIDs physiologic stress induced ZE syndrome idiopathic
6 classical features of duodenal ulcers
epigastric pain burning develops 1-3 hours after meal relieved by eating and antacids interrupts sleep periodicity *duodenal ulcers are rarely malignant
*gastric ulcers have more atypical symptoms and a biopsy is necessary to exclude malignancy
investigations for PUD
endoscopy
upper GI series
h pylori tests
fasting serum gastrin measurement if ZE suspected
approach to PUD
stop NSAIDs
acid neutralization
h pylori eradication
quit smoking
management of bleeding peptic ulcers
EGD to explore upper GI tract
IV panto drip
estbalish risk of rebleeding or continuous bleed since most stop bleeding spontaneously
–increased age above 60, history of PUD, comorbid disease, hemodynamically unstable or endoscopic signs of recurrent bleeding
if high risk for rebleed consider ICU admission
how do NSAIDs cause PUD
direct–> erosions/petechiae via local effect of drug on gastric mucosa
indirect–> systemic NSAID effect–> inhibits mucosal COX leading to decrease synthesis of protective prostaglandins and thus leading to ulcers
risk factors for stress induced gastric ulceration
mechanical ventilation
anticoagulation
multiorgan failure
speticemia
severe surgery or trauma
CNS injury ("cushings ulcers")
burns involving more that 35% of body surfaceWhat does stroke volume depend on?
Preload, after load and contractility
What determines cardiac output
Heart rate and stroke volume
Why is there reduced cardiac output in HF?
Either:
- Impaired ventricular filling–> diastolic failure
- Impaired ventricular ejection–> systolic failure
What is systolic heart failure?
HFrEF–>reduced ejection fraction
Decreased myocardial contractility which results in low EF
What is diastolic heart failure
HFpEF–> preserved contractility and EF but with impaired cardiac compliance
Higher filling pressures for a given LV volume–> increased filling pressures reflect back into the pulmonary and systemic circulations which results in overload sx
The ventricle can’t fill adequately and thus you get decreased preload and thus decreased CO–> fatigue, lethargy, ischemia
If the echo is normal with clinical signs of HF you have HFpEF
How do you distinguish between “forward failure” and “backward failure” in heart failure?
- Forward failure = COLD failure
- -usually requires CCU admission as it is more severe
- -heart is not pumping enough blood to meet organs needs–> under perfusion of brain, kidneys, periphery
- -can’t diurese these patients without pressor support - Backwards failure = WET failure
- -fluid backs up because heart “can’t keep up”
- -volume overload–> pulm edema, SOB, peripheral edema
What are the two defining characteristics of systolic dysfunction? With these in mind, what can cause systolic dysfunction?
- Impaired contractility–> myocardial ischemia/infarction, chronic volume overload, dilated cardiomyopathy
- Increased after load–> aortic/pulm stenosis, HTN
What are the two defining characteristics of diastolic dysfunction? With this in mind, what can cause it?
- Impaired relaxation–> LVH, HOCM, restrictive cardiomyopathy, MI
- Obstruction to filling–> mitral/tricuspid stenosis, pericardial constriction, tamponade
What is the pathophysiology behind CHF?
Decreased CO leads to activation of the RAAS and sympathetic systems, which further exacerbates CHF
CHF is a disorder of neurohormonal dysregulation
Sympathetic stimulation–> vasoconstriction–> increased after load
RAAS stimulation–> fluid retention–> volume overload
What are some causes of restrictive cardiomyopathy?
Sarcoidosis, amyloidosis, hemochromatosis
What are the different classes that make up the NYHA classification system for heart failure?
I–sx with extraordinary activity
II–sx with ordinary activity
III–sx at less than ordinary activity
IV–sx at rest
What is a mnemonic for causes of acute CHF exacerbation?
FAILED
Failed to take meds Anemia, arrhythmia Ischemia, infection, infarction Lifestyle indiscretion--increased salt or fluid intake Endocrine (TSH), EtOH Drugs (NSAIDs, steroids)
What types of things should you ask on history for heart failure?
- Characterize the symptoms
- -dyspnea, Orthopnea, PND
- -pedal edema, ascites, RUQ pain (liver congestion)
- -fatigue - Investigate the cause
- -Hx of HTN, CAD, valvular disease, arrhythmias
- -cardiac risk factors
- -Hx of anemia, thyroid disease, pregnancy
- -recent flu–?myocarditis
- -EtOH
- -family history of dilated or hypertrophic cardiomyopathy or of hemochromatosis
What should you be looking for in particular on a physical exam for HF?
- ABCs/general/vitals
- -BP, tachy/Brady, hypoxia
- -WOB, cyanosis - Respiratory
- -crackles, wheezes - CVS
- -volume assessment (JVP, peripheral edema)
- -apex (may be dilated or displaced in a dilated cardiomyopathy, may be sustained in hypertrophic cardiomyopathy)
- -S3, S4, murmurs - Abdo
- -ascites, hepatomegaly
What labs would be appropriate to order in the setting of heart failure?
CBC–anemia causes high output HF
Lytes, BUN, Cr–baseline before giving diuretics, ACEi
LFTs–elevated with hepatic congestion
If you suspect infiltrative disease:
–calcium level (elevated in sarcoidosis, MM)
–SPEP/UPEP (MM)
–iron studies (hemochromatosis)
TSH is suspect hyper or hypothyroid
BNP–elevated in CHF (also elevated in PE, pulm HTN, LVH, Afib, ACS, renal failure)
What might you be looking for on ECG in the context of heart failure?
Active ischemia or arrhythmia
Old ischemia or conduction disease
LVH, atrial enlargement
What mighty you look for on CXR in the context of heart failure?
- Cephalization of vasculature
- Effusions
- Cardiomegaly
- Kerley B lines
- Bat winging–perihilar fullness
- Peri-bronchial cuffing
What imaging tests may be appropriate to order beyond a CXR in HF?
- Echo–EXAM
- -looks at EF, relaxation
- -chamber sizes, valve anatomy
- -pericardium - MIBI
- Cardiac MRI
- PET
- Coronary angio for CAD
What are the best indices for CHF dx as per the JAMA article?
- HX of CHF
- Clinical gestalt
- S3
- Elevated JVP
- Pulmonary edema on CXR
- Afib
- BNP <100 RULES CHF OUT
What is the acute management of CHF?
L(M)NOP Loop diuretic--lasix (Morphine--no longer recommended) Nitroglycerin--vasodilator O2 above 90% Position upright Positive pressure ventilation (BiPAP--decreases need for intubation and ICU)
What orders should you write for a patient presenting in CHF?
Diet--restrict salt to less than 2g/day and fluid <1.5L/day Frequent vitals Maintain O2 above 90% Daily weights Fluids in and out Furosemide IV BID--reassess daily
What are the goals of chronic CHF management
Decrease mortality, morbidity and hospitalizations
Improve quality of life
What lifestyle elements can help in the chronic management of CHF
Diet–restrict salt and fluid
Quit smoking and drinking alcohol
Exercise–cardiac rehab program
What drugs should be used in the chronic treatment of CHF
- ACEi
- -improve survival
- -improve NYHA class, slow progression of disease
- -attenuate LV remodelling
- -SEs = cough, angio edema, hyperkalemia and elevated Cr–> check writhing 3-5 days of starting - ARBs
- -as effective as ACEi for patients who cannot tolerate ACEi - Beta blockers
- -NOT for acute HF because they suppress the tachy that is compensating for decreased heart function
- -improve survival (metoprolol, bishop roll, carvedilol)
- -improve NYHA and slow progression
- -SEs = Brady, heart block, bronchoconstriction, initial worsening of CHF, hypotension, fatigue, sexual dysfunction
- -metoprolol 100 mg PO BID
- -carvedilol 25-50 mg PO BID
- -bishop roll 10mg PO daily
* *start at 1/4 dose and titration up - Aldosterone antagonists–> spironolactone
- -improves survival
- -indicated for NYHA III-IV, EF <40%
- -improves NYHA
- -SEs = gynecomastia, breast tenderness, AKI, hyperkalemia
- -spironolactone 25-50 mg PO daily - Digoxin
- -NO survival benefit
- -decreases hospitalizations
- -SEs = cardiac arrhythmias, GI disturbance, neutron changes (visual) - Loop diuretics
- -NO survival benefit–used only for chronic treatment if chronically volume overloaded
- -symptomatic benefit
- -SEs = hypotension, volume depletion, hypokalemia, elevated Cr
- -furosemide 20-40 PO BID - Vasodilators
- -hydralazine + nitrate combo for after load reduction if ACEi or ARB intolerable (I.e renal impairment)
- -mortality benefit ESPECIALLY IN AFRICAN AMERICANS
Which drugs used on the management of chronic CHF have survival benefit?
ACEi/ARB Beta blockers (not in acute) Spironolactone (aldosterone antagonists)
Which drugs used in the management of chronic CHF have no survival benefit?
Digoxin–decreases hospitalizations
Loop diuretics–symptoms management if volume overloaded
What are the three principles of diastolic heart failure management
Treat comorbidities
Rate control Afib
BP control HTN
What are some non-drug therapies to manage CHF?
- Implantable defibrillators (AICD)
- -survival benefit for Class III-IV on maximal medical therapy - Cardiac resynchronization therapy (CRT)
- -survival benefit for class III-IV with WIDE QRS on maximal medical therapy - Heart transplant
