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Medical Physiology > kidney PATHO > Flashcards

kidney PATHO Flashcards

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USMLE® Step 1 flashcards
1
Q

What is assessed to localize cause of UT pain?

A

Location, onset, quality, quantity, pattern

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2
Q

Location of bladder?

Location of Urethrea

A

Suprapubic to thigh

In groin/genital region

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3
Q

Are renal and ureters not changed by changing body position?

A

Yes

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4
Q

What is nephralgia?

A

Renal pain

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5
Q

Why is most UT pain referred?

A

Kidney has no pain receptors, damage without nephralgia

capsule is innervated tho!

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6
Q

Pain in lower portions usually indicative of what?

A

obstruction

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7
Q

Urinalysis indicators of urine

A

starting point for DDX

Color, odor, turbidity
Dark, strong smelling = decreased renal func

cloudy/pungent= infection

dipstick test and microscopy needed

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8
Q

TYPES OF RENAL DISORDERS

CONGENITAL

INFECTIOUS

A

Congenital: Renal agenesis, PKD

Infectious: pyelonephritis

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9
Q

——Renal Agenesis——

Definition?

A

Absence of one or both kidneys at birth

- can be isolated problem or assoc with other unrelated disorders

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10
Q

——Renal Agenesis——
Unilateral prognosis?

Bilateral prognosis?

A 
Unilateral prognosis is good, normal single kidney, normal life. 
    compensatory 
     hypertrophy occurs.  
     Issue is when single 
     kidney is abnormally 
      formed
Bilateral prognosis is called POTTER SYNDROME; 75% male 
    abnormal development, 
        or failure to develop
     specific group of facial 
       anaomolies 
     infants die of resp 
        disease
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11
Q

—–PKD—–
Disease is result of?
ARPKD vs ADPKD

A 
PKD is result of multiple dilation of collecting ducts 
      appear as fluid filled 
       cysts 
ARPKD: infants/children 
ADPKD: adults
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12
Q

—–ARPKD—–
What type of genetic disorder?
what chromosome?

A 
Autosomal recessive 
   chromosome 6
   low survivability 
      accompanied by hepatic 
      fibrosis
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13
Q

—–ADPKD—–
Chromosome # defect?

Describe pathology?

On sent of symptoms?

A

Defect on chromosome 16 or 4

Pathology not understood 
    tubular epithelia cell 
    hyperplasia-primary 
    cause- cysts involve 
    entire nephron
On set at 30-50 yrs of age

UTI, back/flank pain, hematuria, htn

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14
Q

Infectious disorders of kidneys pathology?

A

normally kidneys are protected by acidic pH, prevention of reflux, prostastic secretions. Agents normally introduced by retrograde flow of urine

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15
Q

—–Pyelonephritis—–

What is it?

A

Infection of renal pelvis and interstitium

Hematogenous, lymphatic, urinary

Risk factors: vesicoureteral reflux, pregoo, neurogenic bladder, instrumentation, obstruction, sex trauma

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16
Q

—–Acute Pyelonephritis—–
What is it?

Severity depends on?

Infection spread by?

Inflammatory process description?

Infection CAUSED by?

A

Acute infection with one or both upper urinary tracts

severity increases with age

infection prob spreads by ascending microorganisms

Inflam process focal and irregular: pelvic, calyces, medulla

Infection caused by medullary infiltration of WBCs with renal inflammation, edema, purulent urine 
    inflam damaged tubule 
    cells 
     Necrosis of renal papille 
      can happen
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17
Q

—–Chronic Pyelonephritis—-

A

Persistent and recurring episodes of acute that lead to shrunken fibrotic kidney

parenchyma mostly replaced by fibrotic tissue

more likely when infection related to obstruction

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18
Q

—Obstructive disorders—

Pathology?

Urine stasis d/t?

Can be congenital or aquired!

A

Pathology is obstructions interfere with urine flow

Dilation of proximal tract

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19
Q

—–Hydroureter—–
Caused by?
Patho?

Partial obstruction?

A

Caused by complete obstruction

Pathology: pressure in pelvis and tubules increase, GFR fails, BF drops (parts become ischemic), after 4 weeks tubular atrophy and medullary destruction

Partial obstruction - little disruption, but b/l cause fluid retention

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20
Q

-Post obstructive diuresus-

A

After correction
excretion of NA, urea, water
Complications: infection, sepsis, progressive loss of renal function, renal failure

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21
Q

—–Renal Calculus—–
aka what?

Nephrolithiasis?

Pathology?

Ureteral colic

A

Kidney stones: crystals of organic materials

Migrate down urinary tract
pain, obstruction
infection

Presence of stone anywhere in tract

Pathology not well understood

No s/s when in pelvis. pain when in the ureter, ureter distends behind stone

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22
Q

Formation factors for kidney stones?

A

Supersaturation, abnormal urine pH, low urine volume

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23
Q

—–Tumors—–
3 types
Patho?

A

Benign, primary neoplasms, secondary neoplasms

Distort kidney and renal architecture

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24
Q 
Benign renal tumors: 
Oncocytomas
Mesoblastic nephroma
Renal angiomyolipoma 
Renal Adenoma
A

only rep small percent
oncocytomas-genetic, slow growing. Asymptomatic

Mesoblastic Nephroma- benign congenital tumor of infancy

Renal angiomyolimpoma
adults- abdominal bv, adipocytes, smooth muscle

Renal adenoma-common
may be premalignant adenocarcinoma

25
Q

—–Renal Cell Carcinoma—-
aka

risk factors

grow from?

S/s?

A

renal adenocarcinoma
adults 50-70, males
RFs: occupation, high protien diet, smoking, obesity, htn, fam hx

from epithelium of PCT!

hematuria, flank pain, mass

26
Q

—-urothelial tumors—–

Malignant!

A

lining of renal pelvis, calyces, ureter, bladder

baldder- transitional cell carcinoma and squa cell carcinoma, adenocell carcinoma

RF: smoking, coffee, aromatic/amine exposure, uti, fam hx

27
Q

—–Nephroblastoma—–
Aka?
most common?
chromosome defect #?

A

wilm’s tumor
Most common ab tumor in children

defect on chromo 11

28
Q

Glomerular abnormalities

primary vs secondary

A

alteration in structure and function of glomerular capillaries

Primary glomerulopathies: kidney only organ affected

Secondary glomerulopathies: drug exposure, infection, glomerulular injury setting ofmultisystem or vascular abnormalities

29
Q

—–Glomerulonephritis—–

A

inflam of glomerulus

many causes, most common is renal disease/renal failure

30
Q

–Acute glomerulonephritis–
Inflam d/t?

s/s

patho?

A

group a post strep infection!

hematuria, red cell casts, proteinuria, decreased gfr, oligouria, edema, htn

inflamm thickens glomerular membrane

31
Q

Rapidly progrssing glomerulonephritis

A

subacute, crensentric, extracapillary glomerulonephritis

Crescentic- refers to cellular proliferation in bowmans space- crescent lesions

primarily adults

idiopathic or with other glomeruluar disorders

32
Q

—Goodpasture syndrome–
what is is?
patho?

A

anti glomerular basement membrane disease

antibody formation against capillaries

at dx- renal insufficiency

33
Q

Chronic glomerulonephritis

pathological changes

A

several dz that lead to chronic renal failure

proliferation of mesangial cells

tubular dialation + atrophy

Tubulointerstitial injury

34
Q

—Nephrotic syndrome—

A

excretion of 3.5g or more of protein in urine/ day

charcateristic of glomerular injury

hypoalbumenimia, edema, hyperlipidemia, lipiduria

35
Q

Renal Dysfunction Classification

Renal insufficiency

vs

Renal Failure

vs ESRD

Uremia:

Azotemia:

A

can be acute or chronic, or rapidly progressing

Decline in renal function to 25% of normal

sig loss of renal function

<10% function

Uremia-syndrome of renal failure:

Increaseed serum urea levels
also inc creatinine levels

BOTH INDICATE AN ACCUMULATION OF NITROGENOUS WASTES IN BLOOD

36
Q 
--Acute renal failure--
Define as? 
Assoc with what s/s? 
Reversible? 
Caused by? 
Classified how?
A

defined as abrupt reduction in renal function

usually assoc with oliguria-BUN and creatinine levels elevated

usually reversible if caught early

caused by diff clinical conditions

classified as:
prerenal
intrarenal
post renal

37
Q 
ARF-PRERENAL 
aka
d/t? 
many causes 
complications?
A

aka prerenal azotemia

d/t impaired renal blood flow=gfr drops

failure to restore bp/bv may lead to tubular necrosis or acute cortical necrosis

38
Q

ARF-INTRARENAL
aka
many causes
Acute tubular necrosis

A

intrinsic renal azotemia

most common cause,
postishcemic or nephrotoxic
ischemic form most often after surgery

39
Q

ARF–INTRARENAL
ischemia releases ROS and inflam mediators- cell swelling and necrosis

Nephrotoxic ATN-

WHY IS GFR REDUCED

A

produced by numerous antibiotics
drug accumulate in cortex
necrosis uniform-proximal tubules

TUBULAR OBSTRUCTION, BACK LEAK, ALT IN RENAL FLOW

40
Q

ARF-POSTRENAL

A

RARE

occurs w/urinary tract infection that affect kidney b/l

increase intraluminal pressure proximal to obstructions leads to decreased gfr

41
Q

ARF-Overall phases–

Initiation phase

Maintenance phase

Recovery phase

A

Reduced perfusion or toxicity-evolving injury

established injury and dysfunction-urine output lowest
serum creatinine and BUN increase

when renal injury is repaired

42
Q

CHRONIC RENAL FAILURE

Common causes?

A

irreversible loss of renal function

affects nearly all organ systems

progress steadily to ESRD

Causes: DM, HTN

43
Q

CHRONIC RENAL FAILURE
Progression occurs in stages that correlate with specific s/s

Reduced renal reserve?

Renal Insufficiency?

Renal Failure?

ESRD

A

GFR reduced to 50%, no sympyoms but BUN elevated

GFR severly reduced
mild clinical s/s of renal dysfunction

Azotemia, acidosis, impaired urine dilution, severe anemia, eleoctrolyte imbalance
GFR <20%

Near complete absence of GFR

44
Q

Electrolyte + acid/base imbalances

A

Creatinine/urea clearance

sodium/water balance

phosphate and Ca balance

K balance

Acid/base balance

45
Q

Creatinine and urea

A

if GFR falls, plasma creatinine levels INCREASE
keep increasing as GFR drops, good estimate of changing glomerular function

Urea clerance similar

46
Q

Sodium and water imbalances

A

kidneys lose regulatory capacity for sodium and water

must switch to excretion vs filtration for sodium

now difficult to conserve sodium after GFR <25%

ability to conc urine decreases

47
Q

Phosphate/Calcium imbalances

A

mediated by PTH and Vit D

reduced renal phosphate excretion, decreased production of Vit D

48
Q

Potassium imbalances

A

normally mediated by ALDOSTERONE

Increases = life threatening

49
Q

Acid/Base imbalances

A

metabolic acidosis when GFR <30%

50
Q

Organ system effects

Skeletal/Bone alteration

A

hypocalcemia and bone dz d/t lack of vit d

51
Q

Organ effects

CVS

A

htn may lead to CHF

d/t increase in fluid volume, dyslipidemia

52
Q

Organ effects

Neural fct

A

progressive and nonsecific

mild sleep disorders, impaired conc, mem loss, impaired judgemtn

hiccups, muscle cramps, twitching

asterixis,s exiures, coma

peripheral neuropathy

53
Q

Organ effects

Endocrine/reproductive

A

drop in circulating sex steroids

hyperinsulemia

54
Q

organ effects

hematologic alterations

A

normchromic, normocytic anemia

55
Q

Organ effects

Immuno

A

supression of chemotacis, phagocytosis, antibody production, cellular immunity

56
Q

Organ effects

GI

A

25%v of pts
gastroenteritis
uremic fector

57
Q

organ system

integ

A

d/t other complications

58
Q

proteins, carbs, lipids

A

proteinuria and catabolic state contribute to negative nitrogen balance

muscle protein dimishes, serum albumin, complement, transferin are low

glucose intolerance

hypertriglceridemia

59
Q

Clinical manifestations

A

Uremia- # of s.s caused by decline in renal fucntion with accumulation of plasma toxins

Specific mechansims are unknown

anorexia, nausea, vomiting, diarrhea, weight lossm pruritus, edema, neuro changes

Medical Physiology (4 decks)

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