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)