Medicine GI, CV, Fem/M-Rep, Heme Onc, Pulm, Ren, NS Flashcards
Pt with recurrent episodes of pneumonia, sinusitis, and GI infections should make you think of? What test should you get to establish the diagnosis?
humoral immunity defect -> get serum Ig to establish a diagnosis
renal vein thrombosis is commonly associated with which nephrotic syndrome?
how does it present?
membranous glomerulopathy
presents with typical nephrotic syndrome features caused by hypoalbuminemia: periorbital edema, abdominal disteinsion/ascites, lower extremity edema, proteinuria
renal vein thrombosis: acute onset of abdominal pain, fever, and hematuria
2 major side effects of statins
rhabdomyolysis, can lead to renal failure
slightly elevated transminases
most rapid way to decrease serum K concentration (2)
insulin (effect usually occurs within 15-30min) + glucose to avoid hypoglycemia
K can be shifted intracellularly more quickly than it can be removed from the body. However, because this effect is transient, efforts to decrease the total body K should still be made via
Kayexalate (1-2hrs)
furosemide
ß2 agonist
Rx that have been shown to confer a survival benefit in CHF
ACEi
ARB
ß-blockers
spironolactone
“SAAB”
most common cause of CKD and ESRD requiring dialysis
diabetes
why and when does diabetic nephropathy usually occur?
what other symptoms do patients usually present with?
10-15 years after the onset of type I/II DM
occurs because advanced glycation end products and other inflammatory mediators damage the glomerulus, resulting in proteinuria, glomerular nephropathy, and ESRD
at this point, patients typically have 3+ protein, elevated creatinine, decreased visual acuity, elevated BP, and no active urinary sediment (red/cellular casts) to indicate a different etiology of the proteinuria
What is the PVR in a patient with significant bladder outlet obstruction (ie BPH)?
>50 cc
2 coronary vasodilators
dipyridamole and adenosine
what is the coronary steal phenomenon? What medications are usually employed to test this and what is it used to test for?
dipyridamole & adenosine - coronary vasodilators
CPS - in patients with CAD, the diseased vessels distal to the obstruction are maximally dilated (ie their ability to increase myocardial perfusion is limited). Thus as the non-diseased vessels are dilated by these medications, there is a redistribution of coronary blood flow to non-diseased areas, resulting in diminished perfusion of the diseased segments
used to diagnose ischemic heart disease
Patient w/ UC presents with 6 mo history of fatigue and pruritis.
Albumin 3.8
Tbili 1.7 (slightly elevated)
Alk Phos 816 (elevated)
AST 45 (WNL)
ALT 54 (WNL)
ESR 102 (high)
pANCA (+)
What is your leading diagnosis? How would you confirm it?
Other common presenting symptoms?
Primary sclerosing cholangitis
diagnose with cholangiogram (ERCP or MRCP) - shows multi-focal narrowing with intra-hepatic and extra-hepatic duct dilation
other symptoms are releated to cholestasis - fatigue, pruritis, steatorrhea, fat soluble vitamin deficiencies, metabolic bone disease, hepatic failure
metabolic and electrolyte changes in a patient with bulimia nervosa
treatment and justification of treatment?
chronic vomiting -> volume depletion + HCl loss ->
metabolic alkalosis
hypoklaemia
hypochloremia
trmt: normal saline - restores arterial volume, correct hypochloremia, and increases urinary bicarb excretion
note that metabolic acidosis consists of 2 phases: generation phase (excess bicarb produced) + maintenance phase (process preventing renal bicarb excretion)
- generation phase - due to urinary or GI H+ losses (diuretics, vomiting) or decreased PO intake
- maintenance phase - due to hypovolemia, kidneys perceive decreased effective circulating volume and results in RAAS activation -> reabsorption of Na, K, excretion of H, decreased excretion of bicarb
physiology of metabolic acidosis secondary to an underlying disorder
treatment?
consists of 2 phases: generation phase (excess bicarb produced) + maintenance phase (process preventing renal bicarb excretion)
generation phase - due to urinary or GI H+ losses (diuretics, vomiting) or decreased PO intake
maintenance phase - due to hypovolemia, kidneys perceive decreased effective circulating volume and results in RAAS activation -> reabsorption of Na, K, excretion of H, decreased excretion of bicarb
trmt: normal saline to restore arterial volume, correct hypochloremia, and increases urinary bicarb excretion
rapid association: systolic-diastolic abdominal bruit in a patient with HTN and atherosclerotic disease
renal artery stenosis
rapid association: patient with history of HTN has a medication list that includes lisinopril, HCTZ, amlodipine, metoprolol, aspirin, metformin, and glyburide; current BP is 190/120
renal artery stenosis - note that his BP is still high despite the use of multiple medications
What is SAAG?
What are the implications of this value?
serum-to-ascites albumin gradient
(calculate by substracting peritoneal fluid albumin conc. from serum albumin conc.)
used to assess ascitic fluid to diagnose the etiology
SAAG > 1.1 = portal HTN/cardiac ascites/increased hydrostatic pressures within hepatic capillary beds
SAAG < 1.1 = other etiologies (malignancy, pancreatitis, nephrotic syndrome, tb)
pt presents with fatigue, dark urine; PE shows icteric sclera and skin. Labs shows elevated AlkPhos.
Next best step in management?
get US
elevated alkphos are indicative of cholestasis and these patients should be elevated with an RUQ US to assess for intra- vs extra- hepatic causes of biliary obstruction
(+) biliary dilation -> extrahepatic cholestasis
(-) biliary dilation -> intrahepatic cholestasis
when a patient presents with weight loss, blood in stools, and has a family history of colon cancer, aside from the w/o for colon cancer, what else should the patient be evaluated for?
endometrial cancers.
Why? She has Lynch syndrome (aka HNPCC), and Lynch II is associated with a high risk of extracolonic tumors, the most common of which is endometrial carcinoma, which develops in 43% of females in affected families
Best imaging modality for assessing patients with an acute episode of diverticulitis
CT scan
However, if you suspect a perforation secondary to diverticulitis, an upright xray may be employed to look for free air under the diaphragm
AVOID colonoscop/sigmoidoscopy during an acute episode, as the endoscope can perforate the fragile bowel and lead to massive contamination of the abdominal cavity with fecal material
3 major cardiac causes of arterial emboli
LV thrombus, usually secondary to recent STEMi
atrial thrombus secondary to a-fib
aortic atherosclerosis
most common complication of PUD and how does it present?
hemorrhage - presents as hematemesis +/- melena, though a massive upper Gi bleed may present as hematochezia (usually a sign of lower GI bleed)
other complications: perforation, penetration, obstruction
pre-test probability of coronary artery disease is based on several factors. What dictates a low-risk patient?
These patients typically undergo a stress test, which can be positive or negative. How would you interpret either one?
low-risk: men <40/women <50 with atypical chest pain and ø significant cardiac risk factors (non-smoker, no family hx of premature CAD)
(+) stress test in patients at low-risk for CAD -> likely to be a faslse (+)
(-) stress test in patients at high-risk for CAD -> likely to be a faslse (-)
Hep C is a risk factor for these diseases
cirrhosis
HCC
cryoglobulinemia
glomerulonephritis
What is a parapneumonic effusion and what are they typically caused by?
What are the different types and how are they managed?
type of pleural effusion that arises as a result of apneumonia, lung abscess, or bronchiectasis; can be either
- uncomplicated - exudative (predominately PMNs) effusions secondary to inflammation associated with pneumonia; gram stain is negative for any organisms; resolve with abx
- complicated - bacterial invasion into the pleural space, leading to incr. # of PMNs, decr. glucose levels, pleural fluid acidosis, and elevated LDH; (ie if there is pus, (+) gram stain of pleural fluid, or pH <7.0); resolves with drainage via chest tube
- empyema - accumulation of pus in pleural space; resolves with abx + drainage
rapid association: pleural fluid has a pH of 7.3
management?
empyema
diagnose with CT; removal of fluid by thoracostomy
rapid association: pleural fluid has a glucose of 59
management?
empyema
(anything <60 is indicative of empyema)
diagnose with CT; removal of fluid by thoracostomy
indications for tube thoracostomy
pH < 7.2
glucose < 60
T/F digital clubbing is a feature of COPD
False - it is not a feature of COPD, but is actually suggestive of another etiology (lung Ca, cystic fibrosis)
What is ARDs?
acute hypoxemic respiratory failure characterized by diffuse alveolar damage with pulmonary edema that is not due to heart failure or volume overload
patients develop severe respiratory distress and severe hypoxemia, where the ratio of arterial O2 tension (PaO2) to FiO2 is < 300
What is the FEV1/FVC ratio, VC, and DLCO seen in restrictive lung disease?
FEV1/FVC ratio = normal - increased
VC = low
DLCO = decreased
What is the etiology of Zenker’s diverticulum?
Where does it usually develop?
What is the standard treatment?
upper esophageal sphincter dysfunction + dysmotility
usually develops above the upper esophageal sphincter with posterior herniation btwn the fibers of the cricopharyngeal muscle
trmt: excision and cricopharyngeal myotomy
INR goal of patient with prosthetic heart valves
2.5 - 3.5
INR goal of patient with idiopathic DVT
2.0 - 3.0
4 features of nephrotic syndrome
common complication?
proteinuria >3-3.5 g/day
hypoalbuminemia
edema
hyperlipidemia and lipiduria
common complication: hypercoaguability with risk of venous + arterial thrombosis (commonly renal vein thrombosis, which is most common with membranous glomerulopathy)
Usually due to urinary loss of antithrombin 3, protein C/S, increased platelet aggregation, hyperfibrinogenemia due to increased hepatic synthesis, and impaired fibrinolysis
other complications: protein malnutrition, iron-resistant microcytic hypochromic anemia, increased susceptibility to infection, vitamin D deficiency
patient with history of asthma on inhaled albuterol, steroids, salmeterol, and cromolyn. She is admitted and given nebulized albuterol, IV steroids, and o2.
What do you expect her CBC to look like?
elevated WBC with leukocytosis (PMN predominance)
steroids increase the PMN count by stimulating bone marrow release and mobolizing the marginated neutrophil pool
∆ btwn hypertensive urgency vs emergency?
- urgency - severe HTN w/o symptoms or evidence of end-organ damage
-
emergency - markedly severe HTN associated with malignant HTN or hypertensive encephalopathy
- malignant - long-standing, uncontrolled HTN associated with retinal hemorrhages, exudates, or papilledema; can lead to malignant nephrosclerosis (ARF, hematuria, proteinuria)
- encephalopathy - cerebral edema due to breakthrough vasodilation from failure of autoregulation, results in an insidious onset of HA, N, V followed by non-localizing neurologic sx (restlessness, confusion, seizures/coma) if untreated, can also develop SAH or ICH
severe HTN: ¨≥¨180/120 mmHg
Hypertensive emergency has two subtypes - what are they and what are the defining features?
-
emergency - markedly severe HTN associated with malignant HTN or hypertensive encephalopathy
- malignant - associated with retinal hemorrhages, exudates, or papilledema; can lead to malignant nephrosclerosis (ARF, hematuria, proteinuria); usually seen in patients with long-standing uncontrolled HTN
- encephalopathy - cerebral edema due to breakthrough vasodilation from failure of autoregulation, results in an insidious onset of HA, N, V followed by non-localizing neurologic sx (restlessness, confusion, seizures/coma) if untreated, can also develop SAH or ICH
severe HTN: ¨≥¨180/120 mmHg
Hematuria can be of two etiologies - what are they, what are common causes of each, and what does the UA normally show?
non-glomerular
- gross hematuria
- etiology: cancer, infections, PCKD, nephrolithiasis
- UA: RBC w/o proteinuria
- sx: dysuria, flank pain, renal colic depending on etiology
glomerular
- microscopic hematuria (gross may be present in some)
- etiology: glomerulonephritis or basement membrane disease
- UA: dysmorphic RBCs, RBC casts, with proteinuria
- sx: absent or non-specfiic (low back pain), but commonly has features of nephritic syndrome (hematuria, HTN, oliguria, elevated Cr)
Treatment for patients with dyspnea, orthopnea, PND, bibasilar crackles, hypoxemia
think: pulmonary edema, most likely due to acute decompensated heart failure (which is commonly due to LV systolic or diastolic dysfunction)
mgmt: IV furosemide + supplemental O2
patient presents with long-standing heartburn, significant weight loss, fatigue, and smoking history
next step in management?
think: likely to be esophageal cancer
start with: barium swallow followed by endoscopy; if negative, proceed to CT of chest +/- contrast
management of esophageal cancers
if localized: surgery +/- preop chemo/radioTx; curative
if metastatic: palliative thearpy (ie chemo/radioTx); not curative
How to diagnose toxic megacolon?
how are these patients managed?
plain abdominal x-rays
dilated R or transverse colon (>6 cm), possible air-fluid levels, thick haustral markings that<br></br>do not extend across the entire lumen
≥3 of the following:
fever >38 C (100.4)
pulse >120/min
WBC >10.5
anemia
conservative mgmt: IV F, steroids, broad spectrum abx, bowel rest
subtotal colectomy with end ileostomy if colitis does not resolve
medical emergency b/c it can lead to colonic perforation
how do patients with UC develop toxic megacolon?
UC patients typically have inflammation limited to the colonic mucosa, but sometimes the inflammation can extend to the smooth muscle layer, leading to muscle paralysis and colonic dilation
CMV colitis usually affects which patient population
HIV+
How do R vs L sided colon cancers tend to present?
both associated with ∆ bowel habits
R sided - anemia, FOBT+
L sided - bowel obstruction, constipation, abdominal pain
25 yo M smoker recently diagnosed with UC
annual colonoscopy with biopsies once the disease has been present for at least 8 years (even if the disease is relatively well controlled with medications); total colectomy if dysplasia is detected
UC has an increased risk of colorectal cancers, which is proportional to the duration and extent of the disease
rapid association: WBC casts
tubulointerstitial nephritis
usually drug induced (NSAIDs, diuretics, penicillin derivatives, sulfonamides, rifampin)
most common paroxysmal tachycardia in people without structural heart disease
how is this usually managed?
paroxysmal supraventricular tachycardia (PSVT) - attacks begin abruptly and are characterized by HR in 160-220s; caused accessory conduction pathways that allow re-entry through the AV node
mgmt: vagal maneuvers (valsalva, carotid massage, immersion of face in cold water) increase vagal tone and decrease conduction through the AV node, which can slow the HR and often break the rhythm or adenosine
characteristic levels of AST/ALT in patients with alcoholic hepatitis
AST : ALT > 2, with absolute values < 500 IU/L
major ADR of metformin (2)
lactic acidosis + sepsis
management of patient with hypernatremia
remember that it reflects a water deficit and usually occurs in patients who are debilitated or have altered mental status and cannot have access to free water.
mild cases: D5W 1/2NS
severe cases: 0.9% NS
FEV1/FVC <70% with low DLCO
emphysema
FEV1/FVC <70% with normal DCLO
chronic bronchitis
asthma
FEV1/FVC >70 % with low DLCO
ILD
sarcoidosis
asbestosis
heart failure
FEV1/FVC >70% with normal DLCO
musculoskeletal deformity
neuromuscular disease
normal spirometry with low DLCO
anemia
PE
pulmonary HTN
normal spirometry with increased DLCO
pulmonary hemorrhage
polycythemia
How does the ABG and physical exam differ for patients with CHF vs COPD?
ABG
- CHF: hypoxia, hypocapnia, respiratory alkalosis (secondary to tachypnea)
- COPD: hypoxia, respiratory acidosis
PE
- CHF: decreased breath sounds, bibasilar crackles, history of CAD, uncontrolled HTN,
- COPD: widespread bilateral wheezes
pt recently diagnosed with colon cancer presents with a sudden onset of severe dyspnea and L sided chest pain, followed by syncope. BP 86/50, P 120/min and regular. O2 sat 80% on RA, JVD 13cm
diagnosis?
what would you expect to see on further work-up of this patient?
PE
malignancy/pro-thrombotic state + acute onset of dyspnea, chest pain, tachycardia, hypoxia, and clear lungs = PE
patients with an acute massive PE can present initially with syncope & hypotension (due to low arterial perfusion)
TTE: RV dilation & failure due to RVOT obstruction & increased PVR
EKG: RBBB and R axis deviation
rapid association: patient on anticoagulation presents with arterial + venous thrombsis
heparin induced thrombocytopenia type 2 (“two types - immune-mediated)
venous thrombosis can lead to DVTs, PE, skin necrosis
Arterial thrombosis can lead to acute limb ischemia, organ infarction (mesentery, kidney), and stroke
64 M with type II DM, HTN, HLD, HT, and CKD presents with sharp, L sided CP for the last 24hrs that is worsened by deep breathing and relieved by leaning forward. PE shows friction rub at LLSB, EKG shows asymmetric T-wave inversion
Glu 248, Na 135, K 5.4, BUN 96, Cr 5.1
Diagnosis and management?
uremic pericarditis
common in patients with CKD, esp those with BUN >60 mg/dL
does not present wtih classical EKG findings of pericarditis (diffuse ST elevations)
treatment: dialysis
type of murmur that is typically auscultated in IVDU patients
tricuspid regurgitation - holosystolic murmur that increases with inspiration
first-line therapy for controlling anginal symptoms and improving exercise tolerance in stable angina pectoris
alternatives to patients with contraindications to ß blocker therapy (hypotensive, bradycardic)
ß blockers - reduce myocardial oxygen demand by decreasing the HR and myocardial contractility
alternatives: long-acting nitrates (isosorbide dinitrate or mononitrate) or Ca channel blockers (diltiazem, felodipine)
pt presents with exertional SOB, pounding heart sensation esp if he lays on his left side, and a BP 150/45
Aortic regurgitation
“pounding heart sensation” = AR results in increased LVEDV, resulting in an enlarged LV that is closer to the chest wall, esp in the L lateral decubitus position
widened pulse pressure (150/45)
exertional dyspnea = insufficient delivery of O2 to peripheral tissues
T/F patients suffering from acute pain s/p injury should receive the same standard of pain management regardless of addiction history
TRUE
ex: patient with an extensive history of opioid abuse should still get IV morphine if he is suffering an acute, severe pain
Patient receiving blood transfusion suddenly develops wheezing and progresses to respiratory distress. He becomes hypotensive and soon loses consciousness
what type of patients is this reaction most common in?
what should you do next?
anaphylactic shock
common in patients with IgA deficiency due to the presence of anti-IgA IgG antibodies
stop transfusion -> administer Epi IM, vasopressors, histamine blockers, steroids, mechanical ventilation
most common adverse reaction to blood transfusion
when and why does it occur?
febrile non-hemolytic transfusion reaction
occurs within 1-6 hours of transfusion
occurs because during blood storage, leukocytes release cytokines that when transfused, cause transient fevers, chills, malaise
rapid association: boggy and erythematous nasal mucosa
how do patients typically present?
treatment?
non-allergic rhinitis (NAR) aka vasomotor rhinitis
nasal congestion or stuffiness, post-nasal drip (dry cough), no specific identifiable triggers
IN antihistamine + steroids
how do you differentiate non-allergic rhinitis vs allergic rhinitis?
non-allergic rhinitis - nasal congestion/stuffiness, post-nasal drip (dry cough), and no identifiable triggers (typically negative serum radioallergosorbent test (RAST))
allergic rhinitis - eye symptoms, itching, sneezing, specific triggers
patient presents with colicky flank pain with radiation to the scrotum; CT shows 4mm stones in the R upper ureter.
next step in management?
increase fluid intake >2 L /day - purpose is to increase the urinary flow rate an dlower the urinary solute concentration, thereby preventing stone formation
where is brocas area located?
associated symptoms?
dominant frontal lobe
broken speech PLUS contralateral weakness of the face/extremities due to its proximity to the motor cortex and conjugate gaze deviation to the side of the leson
when is an endoscopy vs PPI indicated for a patient with GERD?
endoscopy if there are “alarm symptoms” - dysphagia, odynophagia, weight loss, anemia, blleeding, recurrent vomiting, male >50, history of smoking
PPI if patients do not meet initial endoscopy criteria
acute management of patients who present with cluster HA
prophylactic management?
100% oxygen = most rapid acting and effective in aborting the pain during an acute attack
verpamil = prophylaxis
what is the hemi-neglect syndrome?
where is the lesion typically located?
patient neglects the LEFT side of a space and responds only to stimuli that comes from the RIGHT side (ie patients may shave only the right side of their face, comb the right side of their hair, etc)
lesion in RIGHT (non-dominant) parietal lobe, which is responsible for apatial organization
patient with acne vulgaris and dysmenorrhea started taking oral contraceptives and becomes icterus. Liver biopsy shows dark granular pigment in hepatocytes
Dubin Johnson Syndrome - disorder of bile secretion that results in conjugated hyperbilirubinemia; liver is B-L-A-C-K!
(pigmented granules are not seen in the hepatocytes of Rotor syndrome)
which nerve dysfunction is most likely responsible for impaired corneal sensation secondary to corneal abrasion?
trigeminal (V1), specifically to the nasociliary nerve mediating teh afferent limb of the corneal reflex
patient recently diagnosed with systemic sclerosis presents with HA, increasing dyspnea, malaise, and nausea. BP 235/117, P 120, Hg is 6.9, Plt 57K, Cr 3.8
diagnosis? what is likely to be seen on the peripheral blood smear?
scleroderma renal crises - HTN + AKI in the setting of systemic sclerosis, usually within the first 5 years of SSC diagnosis
peripheral smear: schistocytes + thrombocytopenia
2 diagnostic tests for Multiple Sclerosis
MRI +/- gadolinium
oligoclonal IgG bands on CSF analysis
patient presents with transient monoccular vision loss, family history of stroke, and carotid bruit
fibromuscular dysplasia - non-inflammatory/non-atherosclerotic condition caused by abnormal cell development in the arterial wall taht can lead to vessel stenosis, aneurysm, or dissection
fibromuscular dysplasia
what is it?
who does it usually affect?
which arteries does it normally affect and what type of symptoms present?
diagnostic test?
non-inflammatory/non-atherosclerotic condition caused by abnormal cell development in the arterial wall taht can lead to vessel stenosis, aneurysm, or dissection
affects women 15-50
commonly involves
renal arteries -> HTN
carotid + vertebral arteries -> HA, pulsatile tinnitis, dizziness, TIA, stroke, amaurosis fugax
diagnostic test: CT angio of the abdomen or duplex US
after a central venous catheter is placed, what should be the next step in management?
get a portable CXR to confirm proper placement of the catheter tip and absence of complications* before administering drugs or other agents through the catheter
arterial puncture, pneumothorax, hemothorax, thrombosis, air embolism, sepsis, vascular perforation, myocardial perforation leading to tamponade
inheritance pattern & clinical features of patients with hemophilia A & B
X-linked recessive - occurs exclusively in males
hemarthrosis
intramuscular hematoma (bleeding into skeletal muscle)
GI/GU bleeding
prolonged PTT
best diagnostic test patient who complains of hearing loss and has multiple cafe au lait spots
acoustic neuroma -> MRI + gadolinium enhancement
histological ∆ btwn Crohn’s and UC
Crohns: non-caseating granulomas
other features of Crohns: can affect any part of the GI tract but commonly limited to terminal ielum, transmural involvement, skipped lesions, cobblestone appearance, creeping fatty appearance of mesentary, fistulas, fissures, perinanal disease
UC: crypt abscesses
other features of UC: limited to the colon/rectum but may sometimes involve the terminal ileum (backwash ileitis); abdominal pain + bloody diarrhea
most common cause of lower GI bleed in an elderly patient
diverticulosis - painless bleeding
colon cancer
ischemic colitis
brisk upper GI bleed (usually presents with hematemesis as well)
colonic AVM
coagulopathy
∆ btwn diverticulosis and diverticulitis
diverticulosis - non-inflammed diverticula, painless bleeding (caused by diverticula eroding into a penetrating colonic artery, resulting in a profuse self-limited bleeding per rectum)
diverticulitis - obstruction of diverticula resulting in abd pain + infectious sx, usually w/o bleeding
68 M with COPD, CHF, CAD presents wtih dyspnea, productive cough, fever x3 days. CXR shows lower lobe infiltrate.
diagnosis? management?
community acquired pneumonia
mgmt: determine if he/she can be managed as out-pt or in-pt using the CURB-65 algorithm (1 pt each, ≥2 = inpatient trmt, ≥4 = ICU admit)
Confusion
Uremia (BUN >20)
tachypnea (RR >30)
hypotension (BP <90/60)
Age >65
common causes of CAP
treatment?
S. pneumoniae
Haemophilius
Atypical organisms (mycoplasma)
for heatlhy patients with CAP: doxycycline or macrolides
for patients requiring hospitalization: broad-spectrum fluoroquinolone (levofloxacin, moxifloxacin) or ß-lactam + macrolide
common acid/base abnormality caused by PE
respiratory alkalosis - patient hyperventilates to overcome hypoxia and V/Q mismatching
what is the mechanism behind heparin-induced thrombocytopenia?
heparin binds to platelet factor 4 (PF4), which triggers IgG antibodies to bind to it. This complex then activates platelets by binding to the platelet Fc receptor -> release of procoagulants -> platelet aggregation, thrombin formation -> arterial + venous thrombosis
Splenic macrophages removes the activated platelet-antibody-heparin-PF4 complexes -> thrombocytopenia
what is the serum and urine osmolality in patients with SIADH?
low plasma osmolality (<280 mOsm/kg)
high urine osmolality (>100-150 mOsm/kg)
ADH draws water out of the collecting ducts -> thereby diluting serum but concentrating urine
patient develops an acute onset of chest pain; EGK shows STEMI in leads II, III, aVF; PE: holosystolic murmur at the apex, bibasilar crackles
diagnosis?
mitral regurgitation secondary to papillary muscle displacement, which can occur acutely as in this case or 2-7 days after the infarct due to papillary muscle rupture
the papillary muscle displacement can lead to an abrupt diastolic volume overload, which causes elevated LVEDP/LV filling pressure -> this pressure is reflected back into teh L atrium and pulmonary circulation, and is responsible for the signs and symptoms of acute pulmonary edema and CHF
40 yo alcoholic presents to the ED with confusion, gait instability, and horizontal nystagmus and conjugate gaze palsy in both eyes with absent ankle reflexes in both legs.
vitamin deficiency?
This triad of encephalopathy, oculomotor dysfunction, and gait ataxia is classic for Wernicke’s encephalopathy, which is the result of thiamine (B1) deficiency secondary to chronic alcoholism
DO NOT CONFUSE WITH COBALAMIN B12 DEFICIENCY, which also causes neurologic deficits, including impaired vibratory and position sense and gait abnormalities (due to DCML degeneration) and mental status changes. Oculomotor symptoms are usually <u>absent</u>
alternatives to heparin in a patient who has developed HIT
direct thrombin inhibitors (argatroban, bivalirudin)
synthetic pentasaccharide (fondaparinux)
Management of a patient with an EKG that shows a first-degree AV block (prolonged PR interval) with normal QRS duration
What if it showed a first-degree AV block with prolonged QRS duration?
First degree AV block with normal QRS duration- due to delayed impulse transmission from atria -> ventricles, usually at the AV node; requires no further evaluation unless there is significant bradycardic symptoms (ie syncope)
First degree AV block with prolonged QRS duration (>120 msec)- due to conduction delay below the AV node, usually in bundle branches; requires further evaluation to determine the site of conduction delay because these have an unpredictable progression to advanced 2nd-deg or complete heart block
