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Block 5 > Week 6 > Flashcards

Week 6 Flashcards

1
Q

If you suspect nephritic syndrome → check C3/C4 levels

  1. What are some differentials for low levels? (what causes these low levels?)
  2. what are some differentials for normal levels?
A
  1. Glomerulonephritis, cryoglobulinemia, SLE, membranoproliferative → All the differentials on low category activate complement which means C3/C4 are used up and result in low levels when analyzing patient samples
  2. Vasculitis, anti-GBM antibodies
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2
Q
  1. Proteinuria: which lab value is common for glomerular disease?
  2. Nephritic syndrome - which filtration barriers were lost (RBC,protein)
  3. Nephrotic syndrome - which filtration barriers were lost (RBC,protein)
A
  1. 4+
  2. both (but affects RBC filtration barrier more)
  3. Just the protein filtration barrier
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3
Q

Nephrotic syndrome

  1. what is the damage in this syndrome?
  2. clinical presentation (2)
  3. urinary findings? (3)
A
  1. podocyte damage → leads to impaired charge barrier which is supposed to prevent albumin from coming into nephron
  2. ankle and periorbital swelling, hypercholesteremia
  3. frothy urine, proteinuria, oval fat bodies (lipids trapped in casts → maltese cross)
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4
Q

Nephritic syndrome

  1. what is the damage in this syndrome?
  2. clinical presentation (3)
  3. urinary findings? (3)
A
  1. glomerular inflammation leads to basement membrane damage (damage to endothelial and mesangial cells) → this leads to hematuria
  2. dark urine, swelling, fatigue
  3. hematuria, RBC casts, proteinuria (<3.5 g/day)
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5
Q
  1. How does Nephrotic Syndrome lead to increased risk of infection?
A
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6
Q

How does Nephrotic Syndrome lead to thrombosis?

A
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7
Q

How does Nephrotic Syndrome lead to increased hyperlipidemia?

A
  1. Hyperlipidemia is common in patients with the nephrotic syndrome. The main cause is probably increased hepatic lipogenesis
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8
Q

How does Nephrotic Syndrome lead to edema?

A

Loss of the proteins from your blood allows fluid to leak out of the blood vessels into the nearby tissues causing swelling.

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9
Q
  1. How does nephritic syndrome lead to Hypertension
  2. How does nephritic syndrome lead to Edema
A
  1. This causes a decrease in glomerular filtration rate (GFR) and, if left untreated over time, will eventually produce uremic symptoms and retention of sodium and water in the body (to increase volume → increase GFR), leading to both edema and hypertension.
  2. the bit of proteinuria can still lead to edema
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10
Q

POST-STREP GLOMERULONEPHRITIS (PSGN)

  1. nephritic or nephrotic?
  2. Pathology?
  3. Presentation (5)
A
  1. nephritic
  2. (Type 3 HSR) Immune complexes deposit in glomerulus and attract neutrophils → this leads to inflammation and destruction in epithelial and mesangial cells (glomerulus)
  3. seen in children after GAS infeciton of pharynx/skin. + peripheral and periorbital edema + cola colored urine + HTN + Hypocomplementemia (low C3/C4)
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11
Q

POST-STREP GLOMERULONEPHRITIS (PSGN)

  1. Histology (which of these images)?
A
  1. enlarged, hypercellular glomerulI
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12
Q

POST-STREP GLOMERULONEPHRITIS (PSGN)

  1. Immunofluorescence - type of appearance (granular/linear)?
  2. does it stain positive for any abs?
A
  1. granular
  2. stains positive for IgG, IgM, C3
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13
Q

POST-STREP GLOMERULONEPHRITIS (PSGN)

  1. Electron microscopy- any special structures?
A

subepithelial humps - showing where immune complexes get deposited and cause effect.

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14
Q

BERGER’S DISEASE/IgA NEPHROPATHY

  1. nephritic or nephrotic?
  2. Pathology?
  3. Presentation
A
  1. Nephritic
  2. increased IgA synthesis → makes IgA immune complex that deposit in the mesangium → this leads to inflammation/damage since this is a type III HSR
  3. repeated episodes of hematuria following days after respiratory/GI tract infections (days is a good indicated it is this bc PSGN takes weeks)
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15
Q

BERGER’S DISEASE/IgA NEPHROPATHY

  1. histology
  2. electron microscopy
  3. immunofluorescence
A
  1. mesangial proliferation (also seen on electron microscopy)
  2. granular appearance with stains positive for IgA
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16
Q

DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS (DPGN)

  1. nephritic or nephrotic?
  2. Pathology?
  3. Presentation
A
  1. nephritic
  2. complication of SLE (lupus) - known as type IV lupus nephritis - subendothelial immune complex deposits (which include anti-dsDNA) in glomeruli and drives immune response via type III HSR
  3. more than 50% of glomeruli are affected (hence diffuse…focal is <50%) _ SLE features like rash, arthritis, etc
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17
Q

DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS (DPGN)

  1. Histology structures
  2. Immunofluorescence
A
  1. “wire looping” of capillaries - looks like thickened, dark purple capillaries
  2. granular appearance - “FULL HOUSE” staining (IgG, IgA, IgM, C3, C1q)
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18
Q

RAPIDLY PROGRESSIVE (CRESCENTERIC) GLOMERULONEPHRITIS (RPGN)

  1. nephritic or nephrotic?
  2. Pathology?
  3. Presentation
A
  1. Nephritic
  2. This is more of a pathologic description because many diseases (including acute renal failure) can lead to this condition. It is a severe form of glomerulonephritis.
  3. rapid onset, fatigue, anorexia
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19
Q

RAPIDLY PROGRESSIVE (CRESCENTERIC) GLOMERULONEPHRITIS (RPGN)

  1. histology
A
  1. shows crescents formed by inflammation of macrophages and also fibrin
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20
Q

RAPIDLY PROGRESSIVE (CRESCENTERIC) GLOMERULONEPHRITIS (RPGN)

  1. Differentiate between Type I, II, and IV in terms of immunofluorescence
A
  1. Type I RPGN - linear IF / anti-basement membrane Abs (type II HSR)
  2. Type II RPGN: granular IF / immune complex deposition (type III HSR)
  3. Type IV RPGN: negative IF / pauci-immune (ANCA positive)
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21
Q

RAPIDLY PROGRESSIVE (CRESCENTERIC) GLOMERULONEPHRITIS (RPGN)

  1. What diseases are associated with Type I, II, and III RPGN?
A
  1. Type I - Goodpasture’s (rare disorder in which your body mistakenly makes antibodies that attack the lungs and kidneys)
  2. Type II - most commonly results as a progression of PSGN and DPGN/SLE
  3. Type III - vasculitis syndrome
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22
Q

Alport Syndrome

  1. Nephritic or Nephrotic?
  2. Pathology
  3. Presentation
A
  1. nephritic- this is genetic (x-linked)
  2. mutations lead to defect in collagen type IV → this is found in basement membrane of kidney, eye, ear
  3. Hematuria, hearing loss, occular disturbances (look for triad and family history)
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23
Q

MINIMAL CHANGE OF DISEASE

  1. Nephritic or Nephrotic?
  2. Pathology
  3. Presentation
  4. tx?
A
  1. Nephrotic
  2. effacement/thinning of foot process leads to loss of negative charge barrier. The damage to the podocyte is cytokine induced (common in children after infection)
  3. selective proteinuria - only albumin will appear in urine
  4. Favorable prognosis and Responds well to steroids
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24
Q

MINIMAL CHANGE OF DISEASE

  1. histology
  2. Immunofluorescence
  3. electron microscopy
A
  1. normal
  2. normal
  3. can see slight podocyte foot process efacement
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25
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)

  1. Nephritic or Nephrotic?
  2. Pathology
  3. Causes and complications?
  4. tx?
A
  1. Nephrotic
  2. Hyaline collagen deposits in glomerulus which causes basement membrane to collapse + foot processes effacement
  3. Usually idiopathic, HIV, sickle cell, etc can be cause — can progress to chronic renal failure
  4. Does not respond to steroids
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26
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)

  1. Histology
  2. Immunofluorescence
A
  1. focal, segmental sclerosis/lesions of collagen which look pink and dense
  2. usually negative → SOMETIMES positive for IgM, C3, C1
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27
Q

MEMBRANOUS GLOMERULONEPHRITIS/NEPHROPATHY

  1. Nephritic or Nephrotic?
  2. Pathology
  3. Causes?
A
  1. Nephrotic
  2. Immune complexes deposit on subepithelial region between podocyte and basement membrane → this disrupts filtration barrier and then podocytes lay down extra BM which leads to thickened glomerular BM
  3. idiopathic (anti-phospholipase A2 Abs), SLE, tumors, HBV+HCV, etc
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28
Q

MEMBRANOUS GLOMERULONEPHRITIS/NEPHROPATHY

  1. histology
  2. immunofluorescence
  3. electron microscopy
A
  1. thickened GBM with absence of hypercellularity
  2. granular appearance (stains positive for IgG and C3)
  3. shows dense deposits and spike and dome appearance
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29
Q

DIABETIC GLOMERULONEPHROPATHY

  1. nephritic or nephrotic?
  2. pathology
  3. histology
A
  1. nephrotic
  2. non-enzymatic glycosylation of GBM → leads to mesangial expansion and leakage of proteins
  3. mesangial expansion, GBM thickening, Kimmelsteil Wilson lesions (eosinophilic - Nodules of pink hyaline material form in regions of glomerular capillary loops in the glomerulus. This is due to a marked increase in mesangial matrix)
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30
Q

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MPGN)

  1. Nephritic or nephrotic?
  2. pathology
  3. How many types?
A
  1. can cause both
  2. thickened GBM and proliferation of mesangial cells+mesangial matrix (all of which create a hypercellular environment - HYPERCELLULAR ENVIRONMENT IS WHAT MAKES THIS DIFFERENT THAN MEMBRANOUS NEPHROPATHY)
  3. Type I and II
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31
Q

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MPGN)

Type I

  1. pathology
  2. immunofluorescence
  3. histology
  4. associated with what other diseases/disorders
A
  1. Type I MPGN: subendothelial IgG immune complex deposition → inflammation / mesangial ingrowth
  2. Presents with granular IF (positive for IgG / C3)
  3. Tram tracking- where basement membrane looks outlined twice
  4. associated with hepatitis B and C infection
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32
Q

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MPGN)

Type II

  1. pathology
  2. immunofluorescence
  3. Electron microscopy
A
  1. electron dense deposits in basement membrane → complement overactivation
  2. Presents with granular IF (negative for IgG)
  3. dark ribbons’ on EM
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33
Q

Fill in the blanks

A
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34
Q

ACUTE TUBULAR NECROSIS (ATN)

  1. pathology
  2. what are the different types
A
  1. sudden damage to tubular epithelial cells due (maybe due to ischemia or drugs)
  2. ischemic ATN and nephrotoxic ATN
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35
Q

ISCHEMIC ACUTE TUBULAR NECROSIS (ATN)

  1. pathology
  2. what parts of the nephron does it affect (2)
  3. causes (3)
A
  1. renal ischemia due to vasoconstriction lowers GFR and can cause tubular epithelial necrosis. — There is LOSS OF TUBULAR CELL POLARITY (in which Na/K ATPase move to luminal side and excrete Na+ → further activates macular densa → leads to more vasoconstriction and ischemia/necrosis)
  2. proximal convoluted tubule and thick ascending limb
  3. hypovolemia, shock, massive bleeding
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36
Q

NEPHROTIC ACUTE TUBULAR NECROSIS (ATN)

  1. pathology
  2. what parts of the nephron does it affect (1)
  3. causes
A
  1. damage to tubular epithelial cells induced by specific substances (drug induced or toxin induced) - drugs include cisplatin, lead, contrast dye – toxins include uric acid, myoglobin (from rhabdomyolysis), ethylene glycol
  2. PCT only
  3. drug and toxin induced
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37
Q

ACUTE TUBULAR NECROSIS (ATN)

  1. What leads to the creation of granular cysts
  2. what does histology of ATN look like? (3)
A
  1. epithelial cells sough off into urine and create casts that look muddy brown in appearance
  2. patchy, focal necrosis of nephron - the lumen has occlusions due to epithelial cells sloughing off - “skip” areas of nephron (areas that are unharmed)
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38
Q

ACUTE TUBULAR NECROSIS (ATN)

  1. what are the phases of ATN (3)
A
  1. Phase I (Injury): initial injury occurs, leading to slight decline in urine output
  2. Phase II (Maintenance): presents with oliguria / hyperkalemia / AG metabolic acidosis / uremia
  3. Phase III (Recovery): presents with polyuria / hypokalemia (overactivity of kidneys)
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39
Q

ACUTE INTERSTITIAL (TUBULOINTERSTITIAL) NEPRHITIS

  1. pathology
  2. presentation (6)
  3. causes (3)
A
  1. inflammation of renal tubules/interstitium - this is due to a hypersensitivity reaction mediated by eosinophils and neutrophils (like an allergic reaction)
  2. fever, rash, hematuria, sterile pyuria, CVA tenderness, urinary eosinophilia
  3. drug induced (sulfonamides, rifampin, penicillin) , infection, systemic diseases

no evidence of nephrotic/nephritic syndrome

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40
Q

CHRONIC INTERSTITIAL (TUBULOINTERSTITIAL) NEPRHITIS

  1. how do the tubules present differently than in acute?
  2. how does BUN:Cr change with chronic NSAID use
A
  1. fibrosis or atrophy of the tubules
  2. mildly increased - symptoms resolve with cessation of NSAID use
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41
Q

RENAL PAPILLARY NECROSIS

  1. pathology
  2. presentation
A
  1. coagulative necrosis (a type of accidental cell death typically caused by ischemia or infarction) of renal papillae (where the openings of the collecting ducts enter the kidney and where urine flows into the ureters) - there is sloughing off of tissue into urine which may obstruct blood flow
  2. gross hematuria without pain, without renal failure, no WBC casts
42
Q

RENAL PAPILLARY NECROSIS

  1. causes
A
  1. phenacetin, diabetes, acute pyleonephritis, sickle cell anemia
43
Q

MULTICYSTIC DYSPLASTIC KIDNEY

  1. pathology
A
  1. abnormal ureteric bud → leads to kidney being replaced by cysts (no renal tissue/absent ureter) . If unilateral the remaining kidney will hypertrophy and can sustain life. If this dysfunction is bilateral - Potter’s sequence occurs and can often lead to neonatal death.
44
Q

AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY DISEASE (ARPKD)

  1. At what time in life does it present
  2. pathology
  3. complications
A
  1. presents in infancy
  2. dilation of collecting duct- leads to enlarged kidneys (abnormal liver and kidneys)
  3. potter’s sequence, HTN, renal insufficiency
45
Q

AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE (ADPKD)

  1. At what time in life does it present
  2. pathology
  3. complications
A
  1. presents in adulthood
  2. numerous cysts in cortex/medulla → leads to enlarged kidneys w/ destroyed parenchyma
  3. CKD, HTN, berry aneurysms, hepatic cysts, etc
46
Q

MEDULLARY CYSTIC KIDNEY DISEASE

  1. pathology
  2. inheritance pattern
A
  1. cysts in collecting duct of medulla → renal fibrosis → small, shrunken kidneys (causes early onset gout and renal failure)
  2. autosomal dominant
47
Q

RENAL CELL CARCINOMA

  1. where in the nephron does this most often arise from?
  2. risk factors
  3. what mutation is associated with this
A
  1. PCT - most common epithelial tumor
  2. male, age 50-70, cigarette smoking, obesity
  3. VHL mutation
48
Q

RENAL CELL CARCINOMA

  1. pathology
  2. presentation
  3. histology
A
  1. originates in PCT → invades renal vain/IVC → mets to the bone/lung
  2. hematuria, palpable abdominal mass, flank pain, fever, weight loss
  3. CLEAR CELL carcinoma (polygonal clear cells fill with lipids/carbs)
49
Q

WILMS TUMOR (NEPHROBLASTOMA)

  1. pathology
  2. presentation
  3. presents in what type of patient
  4. genetics/mutation
  5. what does histology show?
A
  1. proliferation of metanephric blastema
  2. palpable flank mass, hematuria, HTN
  3. children around 3 years old
  4. loss of function WT1/WT2
  5. embryonic glomerular structures
50
Q

RENAL ONCOCYTOMA

  1. Pathology
  2. presentation
  3. what does histology show
A
  1. benign epithelial tumor that arises in collecting ducts
  2. painless hematuria, flank pain, abdominal mass
  3. large eosinophilic cells with abundant mitochondria w/o prenuclear clearing
51
Q

RENAL ANGIOMYOLIPOMA

  1. pathology
  2. type of patient?
  3. associated with what disease?
  4. genetic inheritence
A
  1. benign tumors of vessels/smooth muscle/ fat
  2. young children
  3. tuberous sclerosis (a rare genetic condition that causes mainly non-cancerous (benign) tumors to develop in different parts of the body.)
  4. autosomal dominant
52
Q

TRANSITIONAL CELL CARCINOMA

  1. locations found (5)
  2. risk factors (5)
  3. presentation
  4. treatment (3)
A

MOST COMMON URINARY TRACT TUMOR- MULTIFOCAL/RECURRENT

  1. Urinary tract system, renal calyces, renal pelvis, ureters, bladder
  2. smoking, aniline dyes, workplace exposures, cyclophosphamide, phenacetin
  3. painless hematuria WITHOUT casts in urine
  4. surgical resection, radiation, chemo

image says dysplastic urothelium

53
Q

SQUAMOUS CELL CARCINOMA OF BLADDER

  1. where does it originate/result from
  2. risk factors
  3. presentation
A
  1. rare tumor - results from chronic inflammation of bladder
  2. recurrent kidney stones, recurrent cystitis, UTI with schistosoma haematobium
  3. painless hematuria WITHOUT casts in urine
54
Q

ADENOCARCINOMA OF BLADDER

  1. where does it originate/result from
  2. risk factors
A
  1. very rare tumor - results from glandular proliferation in bladder
  2. urachal remnant, history of cystitis
55
Q
  1. What does pyelonephritis mean?
A
  1. kidney infection
56
Q
  1. What is the most common bacteria to cause UTI?
  2. 2nd most common?
  3. the rest that can cause UTI? (3)
A
  1. E. coli
  2. Proteus mirabilis (produces urease so urine has ammonia scent → can also lead to kidney stones)
  3. Klebsiella, staph saprophyticus, enterococcus faecalis
57
Q

ACUTE CYSTITIS

  1. where is this infection limited to?
  2. presentation
A
  1. infection of urinary bladder
  2. suprapubic pain, dysuria (painful urination), urinary frequency, urinary urgency == (NO SYSTEMIC SYSTEMS)
58
Q

ACUTE CYSTITIS

  1. what lab results indicate acute cystitis (hint: there is variety based on bacterial culprit)
  2. Treatment
A
  1. pos leukocyte esterase (indicates WBCs), positive nitrates (indicates gram negative organisms, pyuria
  2. Enterococcus/staph sapro → show negative for nitrates
  3. tx: nitrofurantoin (first line and used in pregnancy) — TMP-SMX (alternative first line but not in pregnancy)
59
Q

ACUTE PYELONEPHRITIS

  1. where is this infection found?
  2. pathology
  3. presentation
A
  1. infection of kidney (upper UTI)
  2. neutrophils infiltrate renal interstitium → affects cortex
  3. fevers, flank pain, CVA tenderness, nausea, vomiting, chills
60
Q

ACUTE PYELONEPHRITIS

  1. Labs that indicate acute pyelonephritis
  2. complications?
A
  1. positive leukocyte esterase, WBC casts
  2. chronic pyelonephritis, renal papillary necrosis, urosepsis
61
Q

CHRONIC PYELONEPHRITIS

  1. How does this arise? (3)
  2. presentation
A
  1. consequence of recurrent acute pyelonephritis ;;; also can be a consequence of vesicouretal reflex (a condition in which urine flows backward from the bladder to one or both ureters and sometimes to the kidneys- usually in children) ;;; also can be seen with recurrent kidney stones
  2. corticomedullary scarring, blunted calyx, etc
62
Q

Xanthogranulomatous pyelonephritis

  1. What is this a category of?
  2. Pathology
  3. what is most often the cause of this
  4. what bacterial infection can lead to this?
A
  1. Chronic pyelonephritis
  2. grossly orange nodules that mimic tumor nodules in kidney - granulomatous tissue containing lipid-laden/foamy macrophages
  3. proteus infection
63
Q

What are the antibiotics used for lower UTI infection? (3)

A
  1. nitrofurantoin
  2. TMP-SMX
  3. Fosfomycin Trometamol
64
Q

What antibiotics are used for pyelonephritis? (2)

A
  1. Fluoroquinolones
  2. Cephalasporins
65
Q

Nitrofurantoin

  1. bactericidal or bacteristatic?
  2. adverse effects
  3. contraindications
A
  1. bactericidal
  2. GI upset, skin rashes, phototoxicity
  3. Pyelonephritis (upper GI infection), CKD, G6PD deficiency
66
Q

TMP-SMX

  1. bactericidal or bacteristatic?
  2. when is it used?
  3. adverse effects
  4. contraindications
A
  1. bacteriostatic - inhibits folic acid synthesis
  2. Alternative first-line agent for uncomplicated lower UTIs (tends to be cheaper than nitrofurantoin)
  3. SJS-TEN, bone marrow and renal toxicity, etc
  4. ESRD, pregnancy, G6PD deficiency
67
Q

Fosfomycin Trometamol

  1. bactericidal or bacteristatic?
  2. when is it used?
  3. adverse effects
A
  1. bactericidal (inhibits bacterial wall synthesis)
  2. Used in resistant, symptomatic UTI in hospitalized patients
  3. diarrhea, headache, dizziness, etc
68
Q

FLUOROQUINOLONES

  1. bactericidal or bacteristatic?
  2. when is it used?
  3. adverse effects
A
  1. Bactericidal (inhibits DNA topoisomerase)
  2. prostatits and upper UTI infection
  3. tendonitis, GI upset, rash, QT prolongation
69
Q

CEPHALOSPORINS

  1. bactericidal or bacteristatic?
  2. when is it used?
  3. adverse effects
A
  1. bactericidal (beta lactam drug that inhibits cell wall synthesis)
  2. inpatient treatment of upper urinary tract infection
  3. hypersensitivity reaction, nephrotoxicity
70
Q

Differentiate between

  1. Stress incontinence
  2. Urgency incontinence
  3. Overflow incontinence
A
  1. Outlet incompetence, leads to leakage with ↑ intra-abdominal pressure
  2. Detrusor overactivity, leads to leakage with immediate urgency to void (a strong, sudden need to urinate that is difficult to delay)
  3. Incomplete emptying, leads to leakage with overfilling
71
Q

Stress incontinence

  1. Associated with what other scenarios
  2. Treatment:
A
  1. obesity, vaginal delivery, prostate surgery, laughing too hard
  2. pelvic floor muscle strengthening, weight loss, pessaries
72
Q

Urgency incontinence

  1. Associated with what other scenarios
  2. Treatment (2)
A
  1. UTI infection
  2. Anticholinergic agents and Beta-3-adrenergic receptor agonists
73
Q

Anticholinergic agents

  1. what type of incontinence is it used for?
  2. How does it work?
  3. Name of drugs? (4)
  4. Adverse effects?
A
  1. urgency incontinence
  2. Block cholinergic receptors in bladder → relaxes bladder → increases urinary capacity
  3. Oxybutynin, tolterodine, solifenacin, fesoterodine
  4. dry mouth, constipation, dry eyes, etc
74
Q

Beta 3 adrenergic receptor agonist agents

  1. what type of incontinence is it used for?
  2. How does it work?
  3. Name of drugs? (4)
  4. Adverse effects? (3)
A
  1. urgency incontinence
  2. acts on beta 3 adrenergic receptor to relax the detrusor muscle → increases urinary capacity
  3. Mirabegron
  4. HTN, Nasopharyngitis, UTI
75
Q

Overflow Incontinence

  1. what causes this?
  2. associated with what disorders?
A
  1. detrusor muscle underactivity, outlet obstruction
  2. polyuria, benign prostate hyperplasia, MS
76
Q
  1. What is benign prostatic hyperplasia
  2. what are the drug types used to treat this condition? (3)
A
  1. enlarged prostate gland compresses urethra (decreases emptying)
  2. alpha receptor blockers, 5alpha reductase inhibitors, PDE-5 inhibitors
77
Q

alpha receptor blockers

  1. what condition is this drug type used for?
  2. What are drug names in this category
  3. how it functions?
  4. adverse effects?
A
  1. benign prostate hyperplasia
  2. tamsulosin and silodosin
  3. blocks alpha adrenergic receptors → relax bladder neck, prostate, and urethra → pee more easily
  4. retrograde ejaculation, ED, orthostatic HTN
78
Q

5alpha receptor inhibitors

  1. what condition is this drug type used for?
  2. What are drug names in this category
  3. how it functions?
  4. When is it used?
  5. adverse effects?
A
  1. benign prostate hyperplasia
  2. finasteride, dutasteride
  3. inhibits conversion of testosterone → 5DHT which then inhibits prostate growth
  4. When alpha adrenergic blockers alone are working well
  5. reduced libido, ED breast tenderness
79
Q

PDE-5 inhibitors

  1. what condition is this drug type used for?
  2. What are drug names in this category
  3. how it functions?
  4. adverse effects?
A
  1. benign prostate hyperplasia
  2. tadalafil - daily dose
  3. promotes smooth muscle relaxation of urethra/prostate bladder
  4. headache, dizziness, dyspepsia
80
Q
  1. what is nephrolithiasis?
  2. How does it present as?
  3. Risk factors?
  4. What are the types? (4)
A
  1. kidney stones
  2. flank, colicky pain, hematuria
  3. hypercalcemia, hyperuricemia, low urine volume (which increases substance concn)
  4. calcium, struvite, uric acid, cystine stones
81
Q

CALCIUM KIDNEY STONES

  1. what substance is increased?
  2. how does this show on imaging
  3. treatment?
A
  1. calcium oxalate or calcium phosphate
  2. radiopaque (structures appear light or white in a radiographic image)
  3. thiazide diuretic (to reduce urinary Ca2+) or citrate (binds to calcium)
82
Q

CALCIUM KIDNEY STONES

  1. what situations can lead to this (5) (hint one is high calcium levels)
A
  1. high calcium levels
  2. high oxalate levels (crohn’s disease/fat malabsorption, gastric bypass patients)
  3. Ethylene glycol (leads to formation of oxalate)
  4. vitamin C abuse (leads to formation of oxalate)
  5. Increased Na+ intake (increases ECV → decreases RAAs → decreases Na/Ca2+ reabsorption in PCT)
83
Q

STRUVITE KIDNEY STONES

  1. what minerals make up this stones
  2. consequence of what dysfunction?
  3. how does this “dysfunction” lead to stone formation
  4. What special form can stones make?
A
  1. ammonium, magnesium, phosphate
  2. UTI
  3. UTI with urease pos bacteria (like proteus, staph sapro, klebsiella) can hydrolyze urea to ammonia which alkalinizes urine and allows environment for struvite stone formation
  4. stahorn calculi - these require surgery and cannot be pass (forms cast of renal pelvis/calyces)
84
Q

URIC ACID KIDNEY STONES

  1. What conditions lead to this?
  2. how does this “dysfunction” lead to stone formation
  3. What special form can stones make?
  4. treatment
A
  1. High uric acid level conditions like gout, leukema, myeloproliferative conditions (which are high cell turnover) +++ seen in chronic diarrhea (more common in hot, arid climates)
  2. there is large amount of uric acid in urine due to #1 and uric acid precipitates → leading to stone formation.
  3. hydration, urine alkalization
85
Q

CYSTINE KIDNEY STONES

  1. consequence of what dysfunction?
  2. What special form can stones make?
A
  1. cystinuria (tubular defect in cystine reabsorption) - most often seen in children (This stone is rare)
  2. staghorn calculi - but this time doesn’t need surgery bc when treatment with hydration and urine alkalization stone can dissolve
86
Q

Determine what each image shows (all have to do with kidney stones)

A
87
Q

EBM

  1. what does a T-test analyze the difference of?
A
  1. used to analyze difference between means of two groups w/ continuous variables
  2. Used in unpaired, independent samples (mean blood pressure between men and women)
  3. Used in paired, dependent samples (mean blood pressure before and after drug administration)
88
Q

EBM

  1. what does a ANOVA analyze the difference of?
A
  1. used to analyze difference between means of ≥ 3 groups w/ continuous variables
    1. Example: blood glucose in type I diabetics / type II diabetics / healthy controls
89
Q

EBM

  1. what does a Chi-square test analyze the difference of?
A
  1. used to analyze difference in proportion of categorical variables in ≥ 2 groups
    1. Example: percentage of males and females who develop subarachnoid hemorrhage
90
Q

EBM

  1. what does a Correlation analysis compare?
A
  1. used to compare relationship between two continuous variables from same subject
    1. Correlation coefficient (r) is between -1 (negative correlation) and +1 (positive correlation)
91
Q

EBM

  1. what does a Regression predict?
A
  1. predicts outcome based on various independent variables
    1. Used to learn about type of relationship between several independent variables and outcome
92
Q

EBM

  1. what does Odds ratio measure?
A
  1. measures association in case control study (how likely is exposure in disease)
  2. Case Control Study: start with disease outcome, look backwards in time to find exposures
93
Q

How do you calculate odds ratio from this?

A
94
Q

EBM

  1. What is efficacy
  2. What is effectiveness
A
  1. Efficacy is the degree to which a treatment prevents disease under ideal and controlled circumstances.
  2. Effectiveness is the degree to which a treatment prevents disease in the real world
95
Q

Fill in the blanks in this table differentiating between an efficacy vs effectiveness study

A
96
Q

Fill in the blanks in this table differentiating between an efficacy vs effectiveness study

A
97
Q
  1. What is surrogate outcome?
  2. What are clinical outcomes?
A
  1. Outcomes that are measurable such as GFR or something the patient really wouldn’t feel/experience
  2. Patient oriented outcomes like death or something the patient can feel/experience
98
Q

EBM

Define these vocab words

  1. temporal relationship
  2. strength of association
  3. Dose-response relationship
  4. consistency
  5. plausibility
  6. experiment
  7. coherence
A
  1. Temporal Relationship: exposure always precedes outcome (essential criteria)
  2. Strength of Association: association strength increases likelihood of causality
  3. Dose-Response Relationship: increased exposure leads to increased risk (not essential)
  4. Consistency: repeated observations in different populations / circumstances show similar results
  5. Plausibility: aligns with current understanding of pathological processes
  6. Experiment: evidences helps establish causality (randomized trials / systematic reviews)
  7. Coherence: coherence between lab + epidemiological findings increase likelihood of causality
99
Q

What is acute tubulointerstitial nephritis?

A
  1. Triad of fever, rash, eosinophilia (in 10% of pts)
  2. pharmaceutical exposures very common → leading to a hypersensitivity reaction to drugs such as penicillins, nonsteroidal anti-inflammatory drugs (NSAIDs), and sulfa drugs
100
Q
  1. Analgesic nephropathy is characterized by what two things?
  2. How do kidneys appear?
A
  1. papillary necrosis
  2. chronic interstitial nephritis
  • all with long term consumption of analgesic agents*
    1. kidneys are small and usually asymmetric w/ bumpy renal contours. Scarring in the pelvis, calyces, or both
101
Q

Polyuria + increased urinary protein combined with nodular glomerulosclerosis (also known as Kimmelstiel-Wilson nodules) indicates what disease

A

Diabetes - recognized in kidney histology

Block 5 (7 decks)

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