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Patho > Renal > Flashcards

Renal Flashcards

1
Q

Key functions of the kidneys

A

Excretion of metabolic waste (urea, creatinine, bilirubin, drugs, hormone metabolites), erythrocyte production via erythropoietin, regulation of water and electrolytes, regulation of BP through RAAS, regulation of acid base (excretion of H ions and reabsorption of bicarbonate), 1,25 dihydroxy vitamins production (calciriol), gluconeogenesis

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2
Q

Renal blood flow

A

In through renal artery, interlobar artery, arcuate arteries, capillary beds, afferent (glomerular capillaries-filtration), efferent (peritubular capillaries-water, lytes. Substance exchange between blood and filtrate making urine), vasa recta (long efferent arterioles-extend through medullary glomerulus to form juxtaglomerular cells, regulate urine and sodium concentration and volume, reabsorb filtrate to return to systemic circulation), out through renal vein

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3
Q

Filtrate and urine movement through kidney

A

Bowman’s capsule, proximal tubule, loop of Henle (descending thin, ascending thick), macula densa, distal tubules (8-10 collecting tubules to form), medullary collecting tubule, collecting duct, renal pelvis

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4
Q

Nephron

A

Glomerulus-glomerular capillaries, fluid is filtered from the blood to form filtrate which enter the tubule
Tubule-tube where filtrate is processed into urine
2 types
Cortical-glomerulus in the outer cortex and tubules that are superficial in the medulla
Juxtaglomerular-glomerulus deep in the cortex that tubes deep into the medulla (vasa recta is here and determines urine concentration)

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5
Q

GFR

A

Determined by hydrostatic pressure colloid oncotic pressure equals natural filtration pressure
Urine is formed as a result of tubular processing of filtrate aka GFR, absorption of substances from the renal tube, built into the blood excretion of substances from the blood to renal tubes

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6
Q

How to increase GFR

A

Hormones and artacoids-local angiotensin two- caused by construction of efferent arterioles increase in blood flow increase in GFR
Nitric oxide, prostaglandins, bradykinin- caused by dilating afferent arterioles increasing blood flow increasing GFR

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7
Q

How to decrease GFR

A

Sympathetic nervous system, nor epinephrine and epinephrine in adrenal medulla-caused by constriction of afferent arterioles decreased blood flow, decreased GFR
Hormones such as endothelin (vascular endothelium)- causes constriction afferent arterioles, decrease blood flow and decreased GFR

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8
Q

Endothelium (fenestrae)in glomerular membrane

A

Function is to regulate vasomotor tone, homeostasis, trafficking of leukocytes

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9
Q

Glomerular basement membrane (collagen and proteoglycans)

A

Scaffold supporting the function of the endothelium and podocytes, problems with basement membrane results in albumin leaking into filtrate

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10
Q

Podocyte of glomerular membrane

A

Filtration slits and slit membrane
The slit serves as a barrier between the foot process to prevent leaking of albumin into the filtrate

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11
Q

Polycystic kidney disease

A

Etiology- autosomal dominate
Patho- polycystine->epithelium, creates cysts->obstructs renal parenchyma
S/s- progression to CKS

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12
Q

Hemolytic uremic syndrome

A

Etiology- most common cause of community acquires AKI in kids, due to ecoli 157 toxin-shiga toxin
Patho- abdominal pain, bloody diarrhea, fever, macroangiopathic, hemolytic anemia (shistocytes), thrombocytopenia, microvascular clots clog glomeruli
S/s-progression to CKD

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13
Q

BPH

A

Etiology- obstruction of urethra
Patho- over distention of bladder leads to hydronephrosis
S/s- overflow incontinence, frequency, UTI, rare AKI/CKD

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14
Q

Chronic glomerular nephritis

A

Etiology-chronic inflammation (slow to develop), diabetic nephropathy, lupus nephritis
Patho-same as acute and podocyte injury, thickening of basement membrane, and glomerulosclerosis
S/s-n/v, hematuria, proteinuria, HTN, edema, decrease UOP

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15
Q

AKI

A

Etiology- pre, intrinsic, post renal
Onset is suddenly
S/s-increase in cr, K, phos, BUN, metabolic acidosis, edema, SOB, fatigue, AMS, muddy urine, decline in GFR due to not enough blood at sufficient pressure for perfusion, UOP and clearance of waste products and lytes
Stage 1-creatinine 1.5-1.9 X baseline or greater than or equal to 0.3 mg/dl
Stage 2-creatinine 2-2.9 X baseline
Stage 3- creatinine 3X baseline or use of renal replacement therapy

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16
Q

AKI Patho pre renal

A

Hypotension, hypovolemia, renal blood flow, renal artery stenosis, abdominal compartment syndrome, usually due to lack of perfusion

17
Q

AKI Patho intrarenal

A

Ischemia, acute tubular necrosis, inflammatory conditions, nephrotoxins

18
Q

AKI Patho post renal

A

BPH, UTU, urinary stricture, indwelling catheter, urinary obstruction, urine unable to drain causing back up

19
Q

CKD

A

Decline in GFR not enough blood to peruse kidneys
Onset insidious
Etiology-chronic injury to nephron, or glomeruli, DM, HTN, glomerulonephritis, PKD, obstruction
Stage 1- severity 90%, GFR greater than 90, mild damage asymptomatic
Stage 2- severity 60-89%, GFR 60-89, mild damage asymptomatic
Stage 3a- severity 30-59%, GFR 45-59, mild to moderate damage but asymptotic
Stage 3b- severity 30-59%, GFR 30-44, some decrease in functional unit, asymptomatic
Stage 4- severity 15-29%, GFR 15-29, severe damage prepare for replacement
Stage 5-severity less than 15%, GFR less than 15, ESRD, kidneys cannot keep up with filtration

20
Q

Complications of CKD

A

Osteodystrophy, decreased vitamin D, HTN, HLD, CVD, decreased insulin, increased parathyroid, anemia, impaired platelets, peripheral neuropathy

21
Q

Nephrolithiasis and urolithiasis

A

Etiology- masses of crystals, proteins, substrates causes obstruction of urinary tract usually unilateral
Patho-salts in urine precipitate and form crystals that grow (calcium oxalate or phosphate, or uric acid, struvite, mg, ammonium)
S/s- pH of urine greater than 7 if calcium, phosphate or struvite
Less than 5 is urine acid, related to movement or obstruction, pain

22
Q

Nephrotic syndrome

A

Etiology- glomerulonephritis, drugs, infection, thromboembolism
Patho-increased permeability through damaged basement membrane
S/s-proteinuria, hypoalbuminemia, edema, HLD, lipiduria

23
Q

Acute glomerular nephritis

A

Etiology- post infectious, autoimmune antibodies found in situ, rapidly progressive glomerulonephritis
Patho- depots of IgG and complexes
Kids-group A beta hemolytic strep
Adults-post staph
IgA nephropathy-deposits of IgA (lupus/early diabetic nephropathy)
Membranous glomerulonephritis
Accumulation of macrophages and proliferation of epithelial cells in bowman’s space form crescents and occludes capillary flow
S/s- fatigue, HTN, edema, ascites, proteinuria, hematuria, decreased UOP

24
Q

Nephritic syndrome

A

Etiology- infection related and rapidly progressive glomerulonephritis
Patho-inflammation of glomerulus
S/s- hematuria, RBC casts, proteinuria less significant, HTN, oliguria

25
Q

Age related changes

A

May hypetrophy as compensatory mechanism due to kidney donation, trauma, disease
Number of nephrons decreases with age beginning at age 40, decreased renal blood flow and GFR
Tubular atrophy-decreased glucose, bicarbonate, sodium reabsorption
Decreased production of vitamin S changes in calcium absorption
Bladder symptoms for common-nephrotic changes and other external causes-hormones, BPH, CVD, position change, diurnal nocturia

26
Q

Blood labs

A

Creatinine clearance-reflects GFR, overestimates function
Cystatin C-marker for renal function, measure of serum proteins filters by glomerulus and metabolized by tubules-elevated levels coordinate with decreased GFR, not affected by infection, diet, inflammation, gender, age, race

27
Q

Urine labs

A

RBC-glomerular nephritis, trauma, stones
WBC-infection
Casts-coagulated proteins, cellular debris, AKI
RBC casts-tubular of glomerular injury
WBC casts- inflammation
Epithelial casts- tubular injury
Broad waxy- status and tubular injury not a good sign

28
Q

Bio markers

A

NGAL-neutrophil gelatinase associated lipocalin-blood and urine
KIM 1-kidney injury molecules 1-urine
IL 18-urine
IGFBIP7- insulin like growth factor binding protein-urine
TIMP2- tissue inhibitor of metalloproteinases 2- urine
Urokinases type plasminigen activator receptor

29
Q

Proximal tubules

A

Reabsorbs sodium, chloride, potassium , phosphate, bicarbonate, glucose amino acids, very water permeable
Secretes- H, organic acids, organic bases (metabolic byproducts, bile salts, uric acid, catecholamines)
Controlled by angiotensin II and PTH

30
Q

Thin descending loop of henle

A

Reabsorbs small amounts of sodium, highly water permeable

31
Q

Thin ascending loop of henle

A

Highly water permeable, dilutes filtrate

32
Q

Thick ascending loop of henle

A

Reabsorbs sodium, potassium, calcium, magnesium, bicarbonate, imperator to water, dilutes filtrate
Secretes H ions
Controlled by angiotensin II, PTH

33
Q

Collecting tubules

A

Reabsorbs sodium, chloride, calcium, bicarbonate permeable to water, ADH requires
Secretes potassium, K, urea
Controlled by aldosterone, ADH, and ANP

34
Q

Medullary collection ducts

A

Reabsorbs urea, water, vasopressin/ADH
Secretes sodium, potassium, H, bicarbonate
Controlled by ADH

Patho (17 decks)

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