Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medical Physiology > kidney PATHO > Flashcards

kidney PATHO Flashcards

1
Q

What is assessed to localize cause of UT pain?

A

Location, onset, quality, quantity, pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Location of bladder?

Location of Urethrea

A

Suprapubic to thigh

In groin/genital region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Are renal and ureters not changed by changing body position?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is nephralgia?

A

Renal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why is most UT pain referred?

A

Kidney has no pain receptors, damage without nephralgia

capsule is innervated tho!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pain in lower portions usually indicative of what?

A

obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TYPES OF RENAL DISORDERS

CONGENITAL

INFECTIOUS

A

Congenital: Renal agenesis, PKD

Infectious: pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

——Renal Agenesis——

Definition?

A

Absence of one or both kidneys at birth

- can be isolated problem or assoc with other unrelated disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A 
Autosomal recessive 
   chromosome 6
   low survivability 
      accompanied by hepatic 
      fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

-Post obstructive diuresus-

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Formation factors for kidney stones?

A

Supersaturation, abnormal urine pH, low urine volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

—–Tumors—–
3 types
Patho?

A

Benign, primary neoplasms, secondary neoplasms

Distort kidney and renal architecture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
-----Renal Cell Carcinoma---- aka risk factors grow from? S/s?
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
----urothelial tumors----- | Malignant!
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
-----Nephroblastoma----- Aka? most common? chromosome defect #?
wilm's tumor Most common ab tumor in children defect on chromo 11
28
Glomerular abnormalities primary vs secondary
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
-----Glomerulonephritis-----
inflam of glomerulus | many causes, most common is renal disease/renal failure
30
--Acute glomerulonephritis-- Inflam d/t? s/s patho?
group a post strep infection! hematuria, red cell casts, proteinuria, decreased gfr, oligouria, edema, htn inflamm thickens glomerular membrane
31
Rapidly progrssing glomerulonephritis
subacute, crensentric, extracapillary glomerulonephritis Crescentic- refers to cellular proliferation in bowmans space- crescent lesions primarily adults idiopathic or with other glomeruluar disorders
32
---Goodpasture syndrome-- what is is? patho?
anti glomerular basement membrane disease antibody formation against capillaries at dx- renal insufficiency
33
Chronic glomerulonephritis pathological changes
several dz that lead to chronic renal failure proliferation of mesangial cells tubular dialation + atrophy Tubulointerstitial injury
34
---Nephrotic syndrome---
excretion of 3.5g or more of protein in urine/ day charcateristic of glomerular injury hypoalbumenimia, edema, hyperlipidemia, lipiduria
35
Renal Dysfunction Classification Renal insufficiency vs Renal Failure vs ESRD Uremia: Azotemia:
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
``` --Acute renal failure-- Define as? Assoc with what s/s? Reversible? Caused by? Classified how? ```
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
``` ARF-PRERENAL aka d/t? many causes complications? ```
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
ARF-INTRARENAL aka many causes Acute tubular necrosis
intrinsic renal azotemia most common cause, postishcemic or nephrotoxic ischemic form most often after surgery
39
ARF--INTRARENAL ischemia releases ROS and inflam mediators- cell swelling and necrosis Nephrotoxic ATN- WHY IS GFR REDUCED
produced by numerous antibiotics drug accumulate in cortex necrosis uniform-proximal tubules TUBULAR OBSTRUCTION, BACK LEAK, ALT IN RENAL FLOW
40
ARF-POSTRENAL
RARE occurs w/urinary tract infection that affect kidney b/l increase intraluminal pressure proximal to obstructions leads to decreased gfr
41
ARF-Overall phases-- Initiation phase Maintenance phase Recovery phase
Reduced perfusion or toxicity-evolving injury established injury and dysfunction-urine output lowest serum creatinine and BUN increase when renal injury is repaired
42
CHRONIC RENAL FAILURE Common causes?
irreversible loss of renal function affects nearly all organ systems progress steadily to ESRD Causes: DM, HTN
43
CHRONIC RENAL FAILURE Progression occurs in stages that correlate with specific s/s Reduced renal reserve? Renal Insufficiency? Renal Failure? ESRD
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
Electrolyte + acid/base imbalances
Creatinine/urea clearance sodium/water balance phosphate and Ca balance K balance Acid/base balance
45
Creatinine and urea
if GFR falls, plasma creatinine levels INCREASE keep increasing as GFR drops, good estimate of changing glomerular function Urea clerance similar
46
Sodium and water imbalances
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
Phosphate/Calcium imbalances
mediated by PTH and Vit D reduced renal phosphate excretion, decreased production of Vit D
48
Potassium imbalances
normally mediated by ALDOSTERONE Increases = life threatening
49
Acid/Base imbalances
metabolic acidosis when GFR <30%
50
Organ system effects Skeletal/Bone alteration
hypocalcemia and bone dz d/t lack of vit d
51
Organ effects CVS
htn may lead to CHF | d/t increase in fluid volume, dyslipidemia
52
Organ effects | Neural fct
progressive and nonsecific mild sleep disorders, impaired conc, mem loss, impaired judgemtn hiccups, muscle cramps, twitching asterixis,s exiures, coma peripheral neuropathy
53
Organ effects | Endocrine/reproductive
drop in circulating sex steroids | hyperinsulemia
54
organ effects | hematologic alterations
normchromic, normocytic anemia
55
Organ effects | Immuno
supression of chemotacis, phagocytosis, antibody production, cellular immunity
56
Organ effects | GI
25%v of pts gastroenteritis uremic fector
57
organ system | integ
d/t other complications
58
proteins, carbs, lipids
proteinuria and catabolic state contribute to negative nitrogen balance muscle protein dimishes, serum albumin, complement, transferin are low glucose intolerance hypertriglceridemia
59
Clinical manifestations
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions