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Block 9 > Week 5 > Flashcards

Week 5 Flashcards

(90 cards)

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1
Q

What females have higher rates of UTI and why?

A

Postmenopausal women have higher rates of infection because of bladder or uterine prolapse and other hormonally induced changes

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2
Q

Cause for increase in UTI in males?

A

Obstruction of the urethra following development of benign prostatic hypertrophy

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3
Q

Most common cause of uncomplicated UTI in all age group

Second

A

E. Coli

S. saprophyticus

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4
Q

Causes for complicated UTi (organisms)

A

E. coli, Proteus mirabilis, Klebsiella pneumoniae, Enterococcus spp., and Group B streptococci

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5
Q

Cause for granulomatous inflammation in bladder wall

Fungal cause

A

Schistosoma hematobium

Candida

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6
Q

Host risk factors for UTI

A

Female

Sex

Benign Prostatic Hyperplasia

Vesicoutheral reflux (bladder ot kidey)

Pregnancy (bladder emptying)

Urethral catheters

Calcui

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7
Q

Where are organisms that cause UTI found in?

A

feces

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8
Q

Virulence factor that facilitates infection UTI

A

fimbrae

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9
Q

anti-UTI factors

A

Urine flow

Uroepithelial cell sloughing,

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10
Q

Types of fibrae

other pathogenic compounds

A

Type I - bind to mannose; cystitis and pyelonephriits

P Fimbrae - bind to glycosphingolipid; pylonephirits

hemolysin (damage to uroepithelium)

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11
Q

Symptoms of cystitis

A

urgency and frequency of urination

voiding small volumes of urine (oliguria)

painful urination (dysuria)

suprapubic tenderness just before or

immediately after voiding

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12
Q

Diagnosis of cystitis

A

uterine pH - dipsitc (not elevated =E.coli / elevated Proteus)

pyuria (WBCs in urine) - leukocyte esterase

bacteriuria (bacteria in urine) - nitrates, clean-catch urine specimen

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13
Q

Cystitis treatment

A

Most get well without antibiotics

nitrofurantoin, trimethoprim-sulfamethoxazole, and fosfomycin

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14
Q

When the cystitis treatment is a must?

A

Pregnant women

Renal transplant

genitourinary tract surgery

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15
Q

Pylonephritits

symptoms

A

fever (>38° C)

nausea and vomiting

flank pain and tenderness

costovertebral angle tenderness

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16
Q

Alternative route to kideny infection

organism?

A

pyelonephritis

hematogenous

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17
Q

Acute vs. Chronic

pyelonephritis

A

Acute

the kidney is somewhat enlarged, and discrete, yellowish, raised abscesses are apparent on the surface

neutrophilic infiltrate, suppurative necrosis, and abscess formation

Chronic

chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis

parenchyma shows interstitial fibrosis with an inflammatory infiltrate of lymphocytes, plasma cells, and occasionally neutrophils

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18
Q

Complications of pyelonephritis

A

Papillary necrosis - diabetics, ssd, urinary tract obstruction

Pyonephrosis - when complete obstrction filling renal pelvis, calyces, and ureter

Perinephric abscess - extension of inflammation through the renal capsule

Xanthogranulomatous pyelonephritis - chronic pyelonephritis characterized by accumulation of foamy macrophages intermingled with plasma cells, lymphocytes, epithelioid cells, and occasional giant cells (associated with proteus)

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19
Q

Proteus

growth pattern

enzye

formation of

A

Swarming growth

urease

Struvite calculi

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20
Q

Treatment of pyelonephritis

Prevention

A

Fluoroquinolone

severe: IV ceftriaxone

High fluid intake ; tannins (cranberry)

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21
Q

Prevention of UTI

A

No spermicide-containg contraceptives

(post-menapausal) oral or vaginal estorgen

Lactobacilli

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22
Q

Prostatitis

symptoms and tests

A

Recal exam - swollen (boggy) prostate, warm, tender

PSA testing

midstream catch

ph, leukocyte esterase, nitrates

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23
Q

Prostatitis

treatment

A

trimethoprim- sulfamethoxazole

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24
Q

Juxtamedullary vs. Cortial nephrone

A

Juxtamedullary hyperosmotic 600-1200 mOsm

Cortial isosmotic 300 mOsm

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25
Diuretics actions
26
Where do all diuretics act? Exception? How weak acids/bases not filtered at glomerules get ito lumen?
Luminal surface of tubules Aldosterone antagonist Organicacid/base transporters
27
What ions are absorbed in PCT
bicarbonate (help of Na+/H+ exhanger) and Cl-
28
Carbonic Anhydrase (CA) Inhibitors Example Result Uses toxicity
Acetazolamie Alkaline urine, more sodium (Na+/H+ exch) glaucoma, metablic alkalosis, altitude sickness, pseudotumor cerebri Hypokalemia, hypercholremic metabolic acidosis, parasthesia, hyperammonemia
29
Mannitol Where action Mechanism Use Side effect Contraindication
proximal tubule and loop of Henle, collecting duct Increase tubular fluid osmolarity Elevated intracranial/intraocular pressure, drug overdos Dehydration Anuria, CHF, pulmonary edema
30
Loop diuretics Example Mechanism Delivery Promote production of what
Furosamide (Laxis) Inhibits Cl-/K+/Na+ (NKCC2) Organic transporter Prostaglanding -- natruresis
31
Reabsorption, Secretion, Excretion in the DCT
Impearmeable to H2O Na+/Cl- by cotransporter (NCC) Ca++ regulated by PTH
32
Thiazide Effective in How gets in Effects on ions Strength Example Use
Both acidic and alkaline condiciton (not like CA) Organic transporter Na+, Cl-, K+, Mg2+ LESS (Ca++ more) Weak Hydrochlorothiazide HT, CHF, hypercalciuria, bromide intox, nephorgenic diabetes
33
Collecting Tubule (CT) Two types of cells
Principal cells - site of aldosterone/vasioressin Intercalated cells - acid-base homeostasis
34
Collecting Tubule (CT) Principal cells function
aldosterone to affect expression of Na+ channels (ENaC) and Na⁺/K⁺-ATPase pumps = Na+ permeability and final K+ in urine Vasopressin action site
35
K+- Sparing Diuretics (Aldosterone Antagonists, Na+ Channel Inhibitors) Examples Use
Sprionolactone, Eplernone, Amiloride, Triamterene HT, CHF
36
Function of ADH
Control water in principal cells ADH regulates the insertion of aquaporin-2 (AQP2) into principal cells in the apical membrane
37
SIADH what is it cause symptom treat
Syndrome of inappropriate ADH secretion (too much ADH) brain injury and bleeding, infection, hydrocephalus, tumors, pulmonary infection, lung cancers (small-cell, mesothelloma), cystic fibrosis Concentrated hypertonic urine Restriction of fluid, correction of hyponatremia
38
SIADH treatment
Demeclocycline (lower the actions of ADH by interfering with the intracellular second messenger cascade) Vaptans (V2 receptor antagonists) Diuretics Osmolarity correction -- fluid
39
Diabetes insipidus (DI) causes
Neurogenic Nephrogenic
40
Neurogenic vs. Nephorgenic DI
Neurogenic (lower ADH lvls) Fluid deprivation test: diluted urine (\<300 mOsm/kg) after water deprivation but \>800 mOsm/kg after AVP or desmopressin Nephrogenic (lower response to ADH) Fluid deprivation test: diluted urine (\<300 mOsm/kg) after water deprivation but \<500 mOsm/kg after AVP or desmopressin
41
Neurologic DI treatment
Arginine vasopressin (AVP) Vasopressin analogs: desmopressin and lypressin (generally IM, SC or intranasally) Chlorpropamide, a sulfonylurea, which ­ actions of ADH
42
Nephrogenic DI
First line: **HCTZ** (↑ Na+ excretion, lower serum osmolarity) and amiloride (↑ Na+ excretion, ¯ Li+ uptake if Li+ toxicity is involved in causing the decreased response) NSAIDS (indomethacin) lower prostaglandin synthesis ↑ ­ response to ADH
43
Tumors of kidney
Hamartomas -- Angiomyolipoma Benign Tumor -- Adenoma (children) and Oncotyoma (adults) Malignant -- Wilm (child) and Renal cell (adult)
44
Where is RCC located? Where is Urothelial Carcinoma located?
RCC - cortex Urothelial - renal pelvis
45
Angiomyolipoma compication composition association
Bleed Blood vessel, smooth muscle, and fat tuberous sclerosis
46
Renal Oncocytoma Origin Appearance Mutation Presentation High denisty of what
intercalated cells of collecting tubules Brown with central scare, well encapsulated 10q Painless hematuria, flank pain, abdominal mass HIgh density of mitochondia
47
Renal Cell Carcinoma Mutation Inheritance Presentation Paraneoplastic Image of clear Color Gene loss
3p- Most sporadic / Von Hippel Linau Triad: flank pain, mass, hematuria + weight loss + paraneoplastic syndromes Syndromes :) Yellow mass VHL (increases IGF)
48
Renal Cell Carcinoma subtyoes
RCC, Clear Cell type: about 75% of all RCC RCC, Papillary type: 10-15% of all RCC RCC, Chromophobe type: 5% of all RCC
49
Renal Cell Carcinoma, Papillary image
50
RCC, Chromophobe image
51
Urothelial Carcinoma Origin Presentation Risk Presentation Spread
Renal Pelvis Calcifications Naphthylamine, azo dyes, cyclphosphamide Painless hematuria Local invasion
52
Wilms Tumor Origin cells
Blastema, epithelium, stromal
53
Beckwith-Wiedemann syndrom
Wilms Neonatal hypoglycemia Muscular hemihypertrophy Organomedally (e.g. tongue)
54
Symptoms of uremia (increased nitro waste in blood) - azotemia
Nausea, anorexia, pericarditis, platelet dysfunctionm, encephalopathy
55
Adult polycystic kidney disease mutations associated problems
PKD1 •Polycystic liver disease •Intracranial berry aneurysms •Mitral valve prolapse
56
Childhood polycystic kidney disease mutation association
PKHD1 Hepatic fibrosis
57
Simple cysts and dialsysi cysts
58
Medullary cysts Appearance Onset Association
Medullary sponge kidney Nephronopthisis Adult-onset medullary cystic disease
59
Vascualr disease: HTN in kidney manifestation
* Benign nephrosclerosis * Malignant nephrosclerosis Renal artery stenosis
60
Thrombotic microangiopathies characteristics two examples
Hemolytic anemia, thrombocytopenia, renal failure HUS and thrombotic thombocytopenic pupura
61
Components of Glomerular basement membrane
Type IV collagen Laminin Heparan sulfate Fibronectin Entactin Glycoproteins
62
Mesangium function
Supports the glomerular tuft and lies between capillaries
63
4 patterns to glomerular injury
Hypercellularity Basement membrane thickening Hyalinosis Sclerosis
64
Description of glomerular injury
* Diffuse: involving all glomeruli * Focal: involving a proportion of the glomeruli * Global: involving the entire glomerulus * Segmental: affecting a part of the glomerulus
65
Acute Renal Failure Characteristics
Azotemia Hyponatremia, Hyperkalemia, Hyperphosphatemia, hypocalcemia Metabolic acidosis Oliguria or anuria
66
Chronic Renal Failure Characteristics Symptoms? Causes
GFR \<60 azothemia, electtrolyte imbalance, uremia Ureami = nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritis, mental status change, visual distrubances DM, HT, Renal parenchymal disease
67
Chronic Renal fail progression
68
Nephritic syndrome: Acute poststreptococcal glomerulonephritis LM IF EM Therapy
Hypercellular Starry sky Subepithelail humps Most children recover, 60% adult recover with fluids
69
Nephritic syndrome characteristics
Inflammatory Hematuria with RBC casts in urine Azothemia, oliguria, HTN Less GFR Periorbital edema Coca-cola
70
Nephritic syndrome: Rapidly Progressive Glomerulonephriits LM/IF Cause
Crescent shape with fibrin¯ophages Goodpasture, SLE, PSGN, small vasculitits Type I (Anti-GBM antibody) - linear IF Type II (Immune complex) - SLE:: EM IgG C3 deposits; IFgranular; wire looping of capilaries Type III (Pauci-immune)
71
Nephritis syndrome:
72
Treatment for a-GBM type 1 Treatment for Type II
Plasmapharesis and immunsuppresion Treat underlying disease, no plasmapharesis
73
Nephritic Syndrome????: IgA nephropathy Importnace Symptom Systemic form LM EM IF presents with
Henoch-schonlein purpura is a systemic form Most common cause of nephrititc syndrome Painless recurrent hematuria in children 1-2 after infection - episodic Mesangial proliferation mesangial IC depositis IF IgA based IC deposits in mesangium Gastroenteritis (gluten enteropathy/liver disease)
74
Location of deposits in diffuse proliferative glomerulonephritis (DPGN)
Subendothelial
75
Alport syndrome Cause Result Treatment
Mutation in IV collagen leading to thinning and splitting glomerular membeane X-linked Glomerulonephirits, dafness, eye
76
Acute Tubular / Kidney Injury (Necrosis) Characteristic Leads to Cause Locations
Decrease in renal function + morpholigic evidance Acute real failure Ischemia (HUS, DIC, vasculitis, hypoTN, shock) Toxic, obstruction
77
Signs of tubulointerstitial nephiritis acute chronic
Histologic: edema, acute inflammatory infiltrate, focal tubular necrosis Mononuclear infiltrate, interstitial fibrosis, widespread tubular atrophy
78
glomerular disease vs. tubulointerstitial nephritis early
metabolic acidosis / inability to concentrate urine
79
Chronic pyelonephritis definition types
Chronic tubulointerstitial inflammation and renal scarring with involvement of the calyces Reflux nephropathy, Chronic obstructive pyelonephritis
80
Light chain nephropathy
Multiple myeloma can affect the kidney Bence Jones proteinuria Amyloidosis Light chain deposition disease
81
Nephrolithiasis
82
Nephrolithiasis
83
Nephrolithiasis types
Calcium oxalate (70%) - hypercalceia Struvite - magnesium ammonium phosphate (15%) - h pylori Uric acid (5-10%) - gout, leukemia, idopathic Cystine (1-2%) - genetic defect absorption of aa
84
Subendothelial
SLE Membranoproliferative glomerulonephritis type 1
85
Sub-Epithelial
PSGN Membranous
86
Focal segmental glomerulosclerosis LM IF EM Cause Steroids MCD
Segmental focus sclerosis and hyalinosis NA Similar to MCD Idiopathic, 2nd (HIV heroin sickle cell obestiy) loss of renal tisuse Variable response Possible evolution stage?
87
Membranoproliferative glomerulonephritis Presentation Type I Type II Association
Nephritic-nephrotic symptoms (either one) or asymptomatic "tram-track" appearance due to GBM splitting caused by mesangial ingrowth Dense deposits Type I - HBV, HCV. activation of the classical and alternative complement pathways SUBENDOTHELIAL Type II C3 nephiritic factor (stabo;oze C3 convertase) -
88
Minimal change disease Most common in Characteristics LM IF EM Association Treat
Children Effacement of podocyte process Normal glomeruli NA Effacement of processes Infection, imunization, immune stiulus, Hogkins Lymphoma Excellent to corticosteroids
89
Membranous nephropathy LM IF EM Most common Cause Steroid
diffuse capillary and GBM thickening granular (similar to sle) Spike and dome Caucasian adults Idiopathic or antibody to PLCA, drugs, SLE, or solid tumors Poor
90
Diabetic nephropathy LM Reactions
mesangial expansion, GB expansion, eosinophlic Nonenzymatic glucosylation of GBM

Block 9 (6 decks)

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