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116 Cards in this Set
- Front
- Back
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Normal blood glucose
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72-144
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normal preprandial fasting level
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<110
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Neurogenic sxs
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sweating
tachycardia tremor irritability nervousness -- autonomic system |
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neuroglycopenic sxs
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HA
droawsiness dizziness blurred vision confusion coma |
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fasting hypoglycemia etiologies
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drugs, insulin & insulin receptor autoantibodies, critical illness, single or multiple organ system failures, malnutrition, sepsis assoc w/ inc glucose utilization, shock, insulinomas
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hypoglycemic drugs
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insulin, SUs (MC cause in elderly), meglitinides, nonselective B-adrenergic antagonists (B-blockers), salicylates & quinine, alcohol--> malnutrition
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early dumping:
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w/n 30 min of eating d/t rapid emptying of food from stomach & duodenum.
assoc w/ large fluid shift into gut lumen-- benign sxs: weakness, diaphoresis & dizziness |
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late dumping:
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1-3 hours after eating; rapid emptying into upper small bowel
sxs: dizziness, lightheadedness, palpitations, diaphoresis, confusion, syncope |
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tx of comatose or confused hypoglycemic pt
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infusion of 50ml IV bolus of 50% glucose
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cornerystone of management of all types of reactive hypogly
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dietary therapy
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most accurate equation at calcultating GFR?
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EPI (serum Cr, age, sex, race)
others: cockcroft/ gault (30-50%) error (age, cr and weight) MDRD-10-20% errors (serum Cr, age, sex , race) |
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CKD defined + stages
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kidney damage or GFR <60 for >3 months
1: GFR >90 2: GFR 60-89 3: GFR 30-59-- largest group-- sent pt to nephrologist 4: GFR 15-29 5: GFR <15 or dialysis |
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MC causes of CKD
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DM, HTN, GN
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complications associated w/ CKD
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anemia, HTN, CVD, DM, Osteodystrophy, malnutition, metabolic acidosis, dyslipidemia
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CKD management of vit D deficiency & phosphate retention
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low phosphate diet
phosphate binders ca not to exceed 2 g/day vit D analogue |
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sxs of anemia
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lethargy
confusion cardiac enlargement angina impaired cognition impaired immune system tinnitus weakness SOB palpitations HA edema, pallor |
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goal for CKD pts
HCO3? pH? |
HCO3: >21 preferably above 23
pH >7.35 |
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how do you evaluate renal disease/ renal function tests
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estimate disease duration
careful UA assessment of GFR |
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assoc clinical findings w/ acute KI
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<3 months, reversible
insult: dehydration, NSAIDS, abs, IV contrast |
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assoc clinical findings w/ chronic KI
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3 months, previously documented inc in BUN & Cr
small kidneys on US or CT IRREVERSIBLE |
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assoc clinical findings w/ acute on chronic RF
assoc clinical findings w/ progressive chronic RF |
acute worsening of renal fxn in a previously stable renal failure
baseline Cr 2 for years & now suddenly 3 or 4 slowly worsening of renal fxn overtime DM |
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casts: what are they indicative of?
RBC? WBC? renal tubular? granular? waxy/ broad? |
RBC: GN
WBC: pyelonephritis Renal tube: atn granular: nonspecific waxy/broad: CRF |
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purpose of GFR
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classify severity
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US what can you assess/ use it for?
IVP? Arteriography? venography? |
size & # of kidneys, mass/cyst
assess obstruction guide in invasive procedures assess bladder for urinary retention assess fxn & structure of urinary tract--- IV contrast arteriography: RAS, uses IV contrast venography: Renal vein thrombosis- dyes |
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nutcracker syndrome
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left renal vein is being compressed by the aorta & superior mesenteric artery
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loin pain hematuria
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young ladies that may have hematuria & flank pain, kidneys tones & even after tx the pain & hematuria remains.
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angiomyolipoma
sickle cell assoc |
benign tumor-- massive hematuria-- pt passing only blood
papillary necrosis |
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heme negative causes of red urine
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rifampin**
phenolphthalein phenazopyridine** ibuprofen beets phosphates bile |
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superntant is red & neg for heme?
supernantant is red & pos for heme? + clear? or + red? |
red & neg= not hemoglobin or myoglobin
red & += hemo or myo red & post + clear= myoglobin red & post + red= hemoglobin |
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extraglomerular: color? clots? proteinuria? RBC morph? RBC casts?
same for Glomerular |
extraG: red or prink, clots may be present, <500 mg/day, normal RBC morph, absence RBC casts
G: red, smoky, brown of "coca cola", absent clots, >500 mg/day, dysmorphic RBC morph, & RBC casts may be present |
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multidetector CT?
multidetector + cytoscopy? cytoscopy? |
MCT: everything in upper tract including tumors & stones & obstructions
MCT + cytoscopy: complete evaluation of GU sysn MCT--> high radiation dose cytoscopy: only way to visualize the prostate & urethra; requires sedation |
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most common cause of outpt hypercalcemia:
MC cause of hypercalcemia in hospitalized pts? |
outpt: primary hyperparathyroid
hospitalized: Malignancy |
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lack of vit D causes:
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secondary hyperparaythryoidism
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Formula for corrected Ca
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Ca + { (4.0 - albumin) x 0.8)}
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#2/#3 cause of hypercalcemia
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milk-alkali syndrome
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familial hypocalciuric hypercalcemia
AD hypocalcemia |
AD, loss of fxn in CaSR in parathyroids & kidneys-- calcium threshold is reset higher, soa higher seum calcium is needed to suppres PTH secretion. (high serum Ca, low urine)
ad hypo: CASR activating mutation--- set point is set lower. ---> want to keep them on a lower Ca. DO NOT DO SURGERY |
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Men 1:
Men 2a: |
1: hyperPTH, pancreatic (gastrin or insulin), pituitary (prolactin)
2a: medullar thyroid cancer, parathyroid hyperplasia, b/l pheochromocytomas |
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tumor markers
myeloma? solid tumors? lymphoma? |
myeloma: Il-6, RANK L
solid tumors: PTHrP lymphoma: extra-renal Vit D 1, 25 OH |
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VITAMINS TRAP
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mneumonic for hypercalcemia
V= vitamins I= immobilization T- thyrotoxicosis A: addison's M- milk alkali I: infection N: neoplasm S: sarcoid T: thiazide R: rhabdo A: AIDS P: Paget's, parenteral nutrition, pheochromocytoma, parathyroi |
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paraythyroid crisis
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marked, severe elevation of calcium & PTH. triggered by another acute process--> onset of diarrhea or another dehydrating etiology
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low calcium + low PTH think:
low calcium + high PTH think: |
AI, hungry bone, abnormal PTH, activating mutation of CaSR, HIV
vit D def, PTH resistance, sepsis, pancreatitis, hyperphosphatemia, pseudohypoparathyroidism (albrights hereditary osteodystrophy), tumor lysis meds: phenytoin, calcium chelators, bisphosphonates |
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magnesium depletion= common cause of hypocalcemia in LT _______
drugs that can cause this? |
hospital pts
cisplatinum, pentamidine, ampotericin B, aminoglycosides, & cyclosporin Mg = cofactor for PTH activity |
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marfan's mutation
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AD on chromosome 15--> codes for fibrillin.
sometimes an activating mutation in TGFBR |
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similar to marfans, but wo vision problems.
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ehlers danlos syndrome
babies: born prematurely 2nd to rupture of fetal membranes |
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vascular EDS
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spontaneous rupture of large arteries & hollow organs-- concern in pregnancy
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defect for ehlers-danlos
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collagen, can be AD, AR, or X linked
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type 3 OI
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pronounced deformity, severly compromised stature, limited mobility, respiratory problems, compression of brainstem
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type IV OI
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reduced stature, some bony deformity, abnormal teeth, normal sclerae
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mutation in OI
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type 1 collagen: COL1A or COL1A2--- AD
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pseudoxanthoma elasticum:
eye & CV |
eye: peau d' orange in retina, spontaneous hemorrhage leads to visual loss
CV: accelerated atherosclerosis, HTN, occlusion & bleeds |
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mutation for pseudoxanthoma elasticum; what should avoid giving these pts?
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AR
ABCC6 gene on chromosome 16 avoid giving gastric irritants- NSAIDS, alcohol |
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GH deficiency sxs- kids
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short stature for age, but normal proportions
delayed growth velocity, bone maturation may have growth deceleration, growth stunting "cherubic faces" fasting hypoglycemia |
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GH adult deficiency
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reduced muscle strength, exercise capacity, lean body mass, bone mineral density
increased abdominal adiposity, body fat mass, glucose intolerance, insulin resistance |
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GH measurement
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IGF-1
if low measure glucose ( insulin induced hypoglycemia); if glucose decreases, GH should rise. |
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non GH deficient short stature
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heigh <-2.25 SD, epiphyses not closed
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GH excess: childhood & adult
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childhood: gigantism
adult: acromegaly --> inc in IGF-1 (d/t benign pit adenoma) |
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acromegaly sxs & complications
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increased morbidity & mortality if untreated, soft tissue, shoe size, bony proliferation, periosteum, "spurs", coarse facial features, enlarged: frontal sinuses & supraorbital ridges; pragnathism, voice changes (d/t incr cartilage in larynx), hyperhidrosis, spade-like hands & feet, TONGUE ENLARGMENT
complications: CHF, ASCVD, CM, arrhythmia, sleep apnea, colonic polyps, tubular adenomas (bigger, more-- right side preferably) |
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acromegaly emergencies
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macroadenoma--- w/ hypotension or CV collapse. --> hypoperfusion & danger.
IV steroids uncontrolled DM visual deficits tx: surgery, or octreotide, lanreotide |
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prolactinoma diagnosis & tx
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dx: micro <10mm, macro >10 mm, snowman appearance on mri, serum prl concentration
>200 ng/ml -- cardinal feature: HA (upon AM arising, occipital, increases w/ cough) tx: dopamine agonists--> bromocriptine, cabergloine |
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ADH & oxytocin-- bound to protein carriers called
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neurophysins-- delivered via intracellular transport
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vasopressinase induced DI
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occurs in 3rd trimester of pregnancy or peripartum:
oligohydramnios, preeclampsia, & hepatic dysfunction an enzyme w/n the blood destroys native vasopressin |
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lithium can cause what type of DI?
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nephrogenic
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primary polydipsia vs DI
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DI urine osmol < plasma
primary polydipsia urine osmol= plasma |
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AI dzes cause what type of DI?
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central-- give DDAVP to tx
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SIADH urine osmol vs plasma
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urine osmole > plasma
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SIADH can only be diagnosed in the absence of? and the presence of?
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absence: nephrotic syndrome, cirrhosis, CHF
presence: normal renal, adrenal & thyroid fxn |
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hyponatremia <110 sxs
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stupor, coma, seizures, focal neurologic changes.
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SIADH causes
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pulmonary: small cell cancer, Tb, pneumonia, abscess
CNS: meningitis, brain abscess, head trauma drugs: C's tumor: lymphoma, sarcoma, pancreatic & duodenal carcinoma |
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tumor marker for medullary thyroid cancer?
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calcitonin
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normal FT4 and decreased TSH= a
increased FT4 & FT3 and normal or increased TSH =b |
a) subclinical/check T3
b) secondary hypothyroidism |
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hot nodule on thyroid scan
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toxic adenoma
solitary, autonomously functioning nodule tx: radioactive iodine |
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patchy increased uptake on thyroid scan
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toxic multinodular goiter: multiple autonomously functioning nodules--> palpable multinodular goiter
tx: radioactive iodine ablation |
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acute thyroiditis
- infection source? - clinical presentation? - PE? - lab? - FNA? tx: |
infection: S. aureus
clinical presentation: systemic manifestations of infection, severe thyroid pain, fever PE: fever, tender asymmetric thyroid, erythema of skin overlying thyroid gland lab: incr wbc and esr fna: polymorphonuclear leukocytes tx: antibiotics |
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Subacute thyroiditis
lab: thyroid scan: tx: |
painful thyroid- MCcause
transient thyrotoxicosis --> transient hypothyroidism lab: elevated ESR, wbc wnl thyroid scan: minimal or absent uptake tx: aspirin or NSAID & propranolol |
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lymphocytic thyroiditis
PE: |
w/n 6 months post partum, thyrotoxix (2-4 wks)--> hypo (4-12 wks)
predisposing factors: previou episode, type 1 DM PE: painless inflammation of gland |
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primary hypothyroidism causes in US & underdeveloped countries
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US: hasimotos
underdeveloped: iodine deficiency AI: sarcoid |
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2ndary hypothyroidism?
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sheehan, pituitary adenoma
aka: pituitary defect |
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normal FT4 & FT3, mildly elevated TSH=a
decreased FT4 & FT3 tsh dec, norm, mildly elevated= b |
a) subclinical- tx if TSH >10 & pos abs
b) secondary/ tertiary * hyperthyroidism |
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causes of cretinism
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abnormality in thyroid dev (dysgenesis or agenesis)
defect in thyroid hormoneogenesis pit or hypothalamic abnormality |
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polyglandular failure syndrome
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AI thyroiditis
AI adrenal insufficency type 1 DM hypogonadism pernicious anemia- b12 vitiligo |
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myxedema coma
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hypothermia, CVA, CHF, infection, drugs
physical findings: altered mental status & hypothemia |
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MC thyroid cancer, assoc with radiation exposure
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papillary thyroid cancer---- tract with thyroglobulin
poor prog: thyroid capsule invasion, nodule > 2.5 cm, pt >45 yo, + LN |
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hurthle cell CA, metastasis to lungs & skeleton
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follicular
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more aggressive than epithelial cancers, less than anaplastic. compnent of MEN 2a & 2b
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medullary thyroid cancer--- flushing, diarrhea, pruritis
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rare, older pop, fna= lymphocytes
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thyroid lymphoma
tx: radiation |
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men 2b; check what gene?
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medullary CA of thyroid, mucosal neuromas, pheochromocytoma
--> triangle + marfanoid habitus check ret-protooncogene |
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normal potassium ECF
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3.5-5.0
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potassium loss can occur as a result of?
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1) shifting K intracellular from ECS: increases post prandial secretion of insulin (K+ uptake by the cell is stimulated by insulin in the presence of glucose, and B-adrenergic stimulation) & alkalosis
2) extrarenal potassium loss (diarrhea, gastric suctioning, chronic laxative abuse) 3) renal potassium loss (aldosterone) 4) decreased K intake summary: you poop it out, pee it out, don't eat it & still give yourself insulin |
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periodic paralysis syndrome
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flaccid episodic weakness or paralysis. hypokalemia assoc.
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what is the most important regulator of body K content?
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aldosterone--- facilitates urinary K excretion thru enhanced K secretion
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myxedema coma triggers & physical findings
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hypothermia, CVA, CHF, infection, drugs
physical findings: altered mental status & hypothemia |
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MC thyroid cancer, assoc with radiation exposure
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papillary thyroid cancer---- tract with thyroglobulin
poor prog: thyroid capsule invasion, nodule > 2.5 cm, pt >45 yo, + LN |
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hurthle cell CA, metastasis to lungs & skeleton
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follicular
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more aggressive than epithelial cancers, less than anaplastic. compnent of MEN 2a & 2b
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medullary thyroid cancer--- flushing, diarrhea, pruritis
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rare, older pop, fna= lymphocytes
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thyroid lymphoma
tx: radiation |
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men 2b; check what gene?
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medullary CA of thyroid, mucosal neuromas, pheochromocytoma
--> triangle + marfanoid habitus check ret-protooncogene |
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normal potassium ECF
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3.5-5.0
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potassium loss can occur as a result of?
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1) shifting K intracellular from ECS: increases post prandial secretion of insulin (K+ uptake by the cell is stimulated by insulin in the presence of glucose, and B-adrenergic stimulation) & alkalosis
2) extrarenal potassium loss (diarrhea, gastric suctioning, chronic laxative abuse) 3) renal potassium loss (aldosterone, diuretics, hypomagnesemia, renal tubular acidosis) 4) decreased K intake summary: you poop it out, pee it out, don't eat it & still give yourself insulin |
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periodic paralysis syndrome
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flaccid episodic weakness or paralysis. hypokalemia assoc.
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what is the most important regulator of body K content? what is an important cofactor for potassium uptake?
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aldosterone--- facilitates urinary K excretion thru enhanced K secretion
magnesium |
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sxs of hypokalemia(severe and not severe)
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muscular weakness, fatigue, muscle cramps, constipation/ileus
severe: flaccid paralysis, hyporeflexia, rhabdo |
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ECG findings of hypokalemia
ECG findings of hyperkalemia |
hypo: decr amplitude, broadening of T waves, prominent U waves
hyper: ECG changes--- peaked T waves, absent P waves, wide QRS sinus brady=== really bad |
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hypok tx:
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mild- mod: oral potassium, replace orally
severe: IV potassium --- while continuous monitoring cardiac. fasting K transfusion rate <40; no more than 80 should be placed in a liter of IV fluid |
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hyperkalemia define & causes
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K level >5.5
severe 7.0 or greater causes: factitious: In-vitro hemolysis (MC), decreased renal excretion (renal insufficiency/ failure, adrenal or aldosterone insufficiency, drugs), increased potassium load (cellular breakdown, potassium containing salt sub, hemolysis, GI bleeding), & decreased cellular uptake of K (acidosis, drugs-- beta blockers, digoxin , succinyl choline) summary: less pee, more bananas, & dec cellular uptake |
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neuromuscular findings of hyperk
cardiac findings |
lethargy, weakness, paralysis & areflexia
cardiac: hypotension, dyrhythmias |
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serum K<6.6 + no ecg signs: tx?
emergent tx: |
kayexalate (if no ecg signs & after emergent tx)
e tx: calcium gluconate--- fastest, but short lived... reduces risk of dev a ventricular dysrhythmia glucose & insulin albuterol-- stim cellualr K uptake diuretics bicarb therapy |
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delivers dietary TG's to peripheral tissue= a
delivers hepatic TGs to peripheral tissue= b delivers hepatic cholesterol to peripheral tissue:c highly atherogenic-- sends cholesterol to periphery= e mediates reverse cholesterol transport form periphery to liver= d |
a= chylomicron
b= VLDLs c= LDLs d= HDLs e= lipoprotein a |
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enzyme required for cholesterol pathway in liver?
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HMG Co-A reductase
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hypertriglyceridemia= a
dysbetalipoproteinemia= b familial combined hyperlipidemia= c hyperlipoprotein a syndrome= d LOW-hdl syndrome= e |
a) genetic lack of lipoprotein lipase. seen in children--> chronic pancreatitis, hyperviscosity & hyperglycemia (d/ t inc VLDL & TGs)
b= genetic defect in marker apoliportein E2= chylomicrons & IDLs; rare in adults, but highly atherogenic--> atherosclerosis & tuberous xanthomas in tendons c= MC -- genetic mosaid, elevations of cholesterol only, TGs only or combo d= overproduction of LPa--> highly atherogenic & poor responsive to tehrapy e= d/t underproduction of HDL scavenger & higher levels of oxidized LDL in serum |
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other disorders which elevate lipids
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nephrotic
DM hypothyroid renal failure metabolic syndrome |
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resins
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dec colesterol, inc triglycerides
keeps chylomicrons out of the gut --- SE: gastric issues |
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statins
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super duper reduce cholesterol by dec production of VLDL
SE: pretty bad myalgias & rhabdo |
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fibrates
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redUC TGS-- by enhancing lipoprotein lipase ctivity
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omega 3
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dec TGs... some benefit in reduction of arrhythmias via membrane stabilization
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niacin
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effectively incr metabolism of both TGs & cholesterol and can raise HDL--> have to use a large dose
SEs: flushing, HA, hyperglycemia, inc gastric acid |
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LDL & TG levels
persons w/ no other risk: w/ 1 or +: w/ metabolic syndrome or diabetes: atherosclerosis: |
a) LDL <160, TGs <150 (all of them
b) <130 c) <100 d) <70 |
