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Patho Module IV

Terms in this set (67)

Afferent Arterioles
Bring blood to glomerulus
Efferent arterioles
Take blood away from glomerulus; wrap around tubules --> renal vein

Resist flow of blood in capillaries
Glomerulus
Circular structure formed by intertwined capillary networks where plasma filtration begins
Bowman's capsule
Epithelial tissue surrounding the glomerulus
Glomerular filtrate
The 20% of plasma and solutes filtered into Bowman's space; contents include H2O, NaCL, H+, HCO3-, urea, glucose, amino acids, some vitamins and drugs
Proximal tubule
First portion to receive plasma filtrate (convoluted and straight tubules)
Distal tubule
Thick ascending tubule connects to this, which connects to the collecting duct
Collecting ducts
ADH works to collect water here; fine tuning of final filtrate that becomes urine occurs here
Renal pelvis
Carries filtrate/urine to ureter to bladder
Podocytes
Layered on blood vessels to control filtration; visceral layer has foot-like projections that interlock with projections from adjacent podocytes
Renal corpuscle
Glomerulus + Bowman's capsule + Bowman's space
Mesangial cells
Provide structural support and phagocytic activity, perform contractile activity through production of vasoactive substances to regulate glomerular blood flow, and secrete extracellular matrix
Vasa recta
Help kidney produce concentrated urine; contain a group of capillaries and vessels in the kidneys
Mechanisms that determine GFR
Filtration: hydrostatic pressure b/w afferent and efferent arterioles
-Just before blood enters efferent arteriole, oncotic pressure becomes great enough that filtration ceases

Net filtration pressure: change in glomerular hydrostatic, glomerular oncotic, or capsular hydrostatic pressure affects the GFR
Myogenic mechanism
Intrinsic ability of afferent arteriole to alter diameter to keep BF constant
-Increased stretch --> vasoconstriction of AA to decrease BF
-Decreased stretch --> vasodilation

When MAP rises out of range, GFR increases --> inappropriate urine elimination

When MAP is below range, GFR decreases to retain waste and excess water
Tubuloglomerular feedback
Juxtaglomerular cells stimulated to release renin by 3 mechanisms

BP in arterioles stimulates stretch receptors in juxtaglomerular cells

Macula densa cells (which secrete paracrines) are sensitive to NaCl concentration of filtrate
-Low NaCl = low systemic BP --> vasodilation to increase GFR and secretion of renin --> Na+ and H2O reabsorption
-High NaCl concentration = high systemic BP --> vasoconstriction to decrease GFR and inhibit secretion of renin --> decrease in Na+ and H2O reabsorption

Beta-adrenergic stimulation
Sympathetic influence
SNS stimulated by severe decrease in systemic BP (resulting from dehydration and hemorrhage)

SNS innervates afferent and efferent arterioles through stimulation of alpha receptors in their smooth muscle walls
Urine concentration of Na+
Differentiation of low renal BF (pre-renal cause of AKI) and intra-renal (acute tubular necrosis)

<20 = intact

>20 = tubules may have lost ability to reabsorb Na+
FeNa
If kidneys are working correctly, body should retain Na+
U/A
Dysfunctional glomerulus --> proteinuria
AKI pre-renal etiologies
Decreased BF to kidney
-GI bleed
-Hemorrhage
-HF
-Renal artery stenosis
-Drugs
-Sepsis
-HyperCa2+
-Cirrhosis/hepatorenal syndrome
-Abdominal compartment syndrome
AKI intra-renal etiologies
Irreversible loss of nephrons d/t renal cell injury
-Ischemic/nephrotoxic tubular injury
-Allergic/NSAID related interstitial nephritis
-Glomerulonephritis
-Thrombotic microangiopathies
-Atheroembolic dx
NSAIDs
Inhibit prostaglandins that vasodilate AA
ACEIs
Inhibit angiotensin II production that constricts EA
Acute glomerulonephritis
Immune response within the glomerulus to a renal or systemic dx process
Chronic glomerulonephritis
Immune response with progressive pattern of irreversible glomerular injury --> CKD
Glomerulonephritis
Damage --> loss of heparin sulfate layer on basement membrane --> loss of negative charge --> increased plasma protein permeability, increased intrarenal hypercoagulability, and proteinuria
Nephrotic syndrome
-More common in kids
-Proteinuria >3.5 g/day
-Loss of colloid osmotic pressure --> pitting peripheral edema, ascites, HTN
Nephritic syndrome
-More common in adults
-Proteinuria <3-3.5 g/day
-Urine RBCs
-Increased hydrostatic pressure d/t NaCl retention
-Increased glomerular capillary destruction
-HTN
-Periorbital edema
Rapidly progressive glomerulonephritis post streptococcal infection
Subepithelial immune complexes activate complement --> inflammation, injury, and proliferation --> damage
Causes of acute tubular necrosis
Death of renal tubular epithelial cells d/t ischemia/nephrotoxicity
-Ischemia --> hypovolemia --> myocardial, pericardial, or valvular dysfunction/arrythmia, sepsis, SIRS, DIC, renal vasoconstriction, and impaired renal autoregulation
Phases of acute tubular necrosis
Initiation: decreased GFR, increased BUN and Cr --> casts and debris obstruct tubules (back leak of filtrate), decreased production of local vasodilators by tubule epithelial cells worsens vasoconstriction, increased cellular Ca2+, free radical formation, membrane breakdown, and cellular death by apoptosis and necrosis

Maintenance: GFR stabilizes over 1-2 week period

Recovery: regeneration of tubular epithelial cells; may have brief autodiuresis as compensatory mechanisms overlap return of function; BUN and Cr return to pre-injury level
Complications of acute tubular necrosis
-Fluid and electrolyte imbalances
-Anemia
-Infections
-Uremia: pericardial inflammation/effusion, N/V, cramping, lethargy, confusion, asterixis, seizure, platelet dysfunction
Post-renal failure
Back pressure is transmitted into glomerulus --> decreased GFR
-Anatomic obstruction: bladder outlet (prostate, pelvic tumor), ureteral (tumor, stones, stricture)
-Tubular obstruction: crystals (ethylene glycol poisoning), drugs (indinavir, methotrexate), proteins (myeloma cast nephropathy)
HTN --> CKD
HTN --> AA vasoconstriction in attempt to reduce glomerular barotrauma --> AA hypertrophy --> decreased BF to glomerulus (atrophy and necrosis) --> glomerular hyalinization --> decreased BF to tubules (also become injured)
-CKD occurs when >50% of nephrons are lost
Autosomal dominant polycystic kidney disease
-Symptoms usually when 30-50 yo, but cysts evident in childhood
-Unilateral cysts can progress to bilateral kidneys
-Progresses to renal failure
-Adults usually present w/ HTN
-Affects male fertility
Autosomal recessive polycystic kidney disease
-Rarer
-May be evident prior to birth
-Symptoms always evident w/n first months of life
-Mitral valve regurg by age 10
-Often liver involved
-Potter facies
Renal cyst formation in PKD
-Polycystin 1 is localized in epithelial cell cilia in renal tubular lumen
-Increased flow --> interaction of polycystin 1 & 2 --> renal cysts
-Tubules dilate and fill w/ glomerular filtrate
-Cysts >2 mm separate from tubules
-Independent cysts fill with NaCl, H2O, and blood (if hemorrhage)
-Interstitial macrophage infiltration and fibrosis --> increased angiotensin II = increased accumulation of extracellular matrix and fibrosis
Kidney cyst formation anomalies
-HA, dyspnea, atrial arrhythmia, stroke, palpitations, systemic and pulmonary edema

-HTN
-Dull back/side/flank pain
-Upper abdominal/RUQ pain in presence of liver/pancreatic cysts
-Acute pain w/ cyst rupture or hemorrhage into cysts
-Abdominal distention
-Palpable nodules on kidneys
-Hematuria
-Frequent UTIs, pyelonephritis, cystitis
-Kidney stones d/t decreased urine flow
-Polyuria w/ inability to concentrate urine
-Chronic renal failure
PKD --> HTN
Ectopic renin production by cystic epithelial cells

Increased angiotensin II in cyst
CKD management
-Hemodialysis: less effective for those who can't handle major fluid shifts
-Periotoneal dialysis
-Renal transplant
Eligibility for renal transplant
-CKD stage 4: GFR 15-29, severely reduced kidney function
-End-stage CKD: GFR <15 or on dialysis
Complications of CKD
-Skin: bruising, pruritus, dry skin, color changes gray to yellowish, dry brittle hair and nails
-Resp: increased RR, Kussumaul resp, crackles, decreased PO2
-Renal: decreased UOP, azotemia, proteinuria, hematuria, hyperuricemia
-GI: anorexia, N/V, halitosis, metallic taste, GIB
-Cardio: HTN, tachy, dysrhythmia, EKG changes, abnormal sounds, retinopathy, fluid retention w/ peripheral edema and/or pulmonary edema
-Neuro: peripheral neuropathy, restless legs, change in LOC, lethargy, confusion, encephalopathy, altered motor function
-Immune: increased risk of infection
-MS: renal osteodystrophy, decreased Ca2+, vit D impairment, hyperparathyroidism, pathologic fractures
-Heme: anemia, weakness, fatigue, pallor, lethargy, bleeding
Diagnosis of prostate CA
-Physical exam including digital rectal exam
-PSA (controversial but good f/u for known CA
-Often asymptomatic until advanced

Complications: bone mets
Phimosis
-Inability to retract foreskin from glans (distal to proximal)
-Poor hygiene or chronic infections
-May require circumcision
Paraphimosis
-Inability to replace or cover glans with foreskin (proximal to distal)
-If severe, emergent surgery to prevent necrosis
Pathophysiology of endometriosis
-Retrograde menstruation: cervix obstruction --> outflow obstruction
-Hematogenous/lymphatic spread
-Coelomic metaplasia: mullerian ducts during fetal development
Clinical presentation of endometriosis
Endometrial tissue outside uterine cavity (usually in ovaries and uterosacral ligaments)
-Spotting
-Painful defecation
-Pelvic heaviness
-Dysmenorrhea
-Infertility
-Dyspareunia
-Sacral backache
-Dysuria w/ +/- hematuria
-Lesions on cervix or vagina
-Cervical motion tenderness
-Tender adenexal masses
-Uterine retroversion
-Sometimes asymptomatic
Diagnosis of endometriosis
-Presumptive diagnosis can be made on clinical hx and exam
-Serum Ca125 elevation (not a sensitive test)
-MRI: endometrial implants
-TVUS: hemorrhagic ovarian cysts
-Laparoscopy: red, brown, white adhesions
-Histological features: epithelium, glands, stroma, macrophages
Treatment of endometriosis
-Start w/ OCPs and NSAIDs
-Offer GnRH analog Lupron
-Arimidex aromatase inhibitor
-Surgery: cauterization/excision, hysterectomy
BV discharge
-Adherent, thin, milky
-pH >4.5
-Positive whiff test: fishy smell
-Clue cells
Candida discharge
-Thick, clumpy, white
-pH <4.5
-Negative whiff test
-Hyphae
Trich discharge
-Frothy grey-green
-pH >4.5
-Positive whiff test
-WBC, flagellated protozoa
PAP smear testing
-3 years after first sexual encounter
-Age 21
-Immunocompromised
-DES exposure
-q 3 years from 21-29
-q 3-5 years >30 (depending on HPV risk)
-Stop if 3 consecutive negative smears with no abnormals w/n 10 years and >65
DD for "bumps on my bottom"
-Painful sores = genital herpes
-Soft and fleshy = condylomata accuminata (HPV)
-Soft and fleshy on vulva and perineum = condylomata lata (syphilis)
-Soft on abdomen = molluscum contagiosum
Common STDs
GC, CT, trich, molloscum contagiosum, HPV, herpes
Not sexually transmitted
BV
HPV
Increases risk of cervical CA
-High risk: 16 and 18 are associated with CA
-Sexually transmitted
-Cofactors for infection: smoking, HIV, parity, OCPs
PID
Causes: vaginal infection --> endocervicitis --> endometritis --> endosalpingitis --> pelvic peritonitis
-Pelvic pain with cervical motion (chandelier sign) and uterine palpation
-maybe fever, elevated WBCs, and current STI

TVUS: +/- hydrosalpinx (blocked fallopain tube
TOA
Interstitial cystitis
Chronic inflammatory condition of bladder characterized by urgency and frequency in the absence of another cause
-Loss of mucosal surface protector of bladder --> increased permeability
-Pain worse w/ full bladder and certain foods
IBS r/t pelvic pain
Chronic relapsing pattern of abdomino-pelvic pain and bowel dysfunction
-Diarrhea, constipation, bloating, mucous stools
MS disorders r/t pelvic pain
-Abdominal wall myofascial pain
-Chronic back pain
-Poor posture
-Fibromyalgia
-Neuralgia of pelvic nerves
-Pelvic floor myalgia
-Peripartum pelvic pain
Other causes of pelvic pain
-Celiac dx
-Neurological dysfunction
-Porphyria
-Shingles
-Sleep deprivation
Adenomyosis
Presence of endometrial glands within the myometrium
-Dysmenorrhea, menorrhagia, enlarged boggy uterus
Primary dysmenorrhea
Pain with menses that usually onsets 1-3 days prior to menses and lasts 1-3 days
-Crampy lower abdominal pain, N/V, diarrhea, HA
Pelvic congestion syndrome
Retrograde flow through incompetent venous valves --> tortuous and congested pelvic and ovarian varicosities
-Pelvic ache that may worsen premenstrually, after prolonged sitting/standing, or after intercourse
Pelvic floor pain syndrome
Spasm and strain of pelvic floor muscles (levator ani, coccygeus, piriformis)
-Chronic pelvic pain, pain in buttocks and down back of leg, dyspareunia
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