Exam Two Flashcards
Describe renal artery stenosis.
In whom is fibromuscular dysplasia common?
What causes HUS?
What causes thrombotic thrombocytopenic purpora?
Often due to atheromatous plaque (most common) or fibromuscular dysplasia (second most common), causes hypertension and elevates renin due to ischemia in the kidney
Younger women
Hemolytic uria syndrome caused by Shiga like toxin of E. coli 0157:H7 (food illness or undercooked meat)
Deficiency of ADAMTS-13 thus large WVF multimers, thus they benefit more from a transfusion
Describe benign nephrosclerosis.
Describe malignant nephrosclerosis.
Symmetric mild atrophy of the kidneys, grain leather appearance on the cortex surface, small arteries with narrow lumens, thickened and hyalinized walls (arteriosclerosis)
Found in patients with sudden malignant hypertension, systemic sclerosis, chronic kidney disease, tends to affect younger men and black patients, suddenly damages the endothelium / causes intima hyperplasia or hyperplastic arteriolosclerosis (onion skinning is classical for endothelial injury) / elevated plasma renin due to poor blood flow to kidneys, and burst petechial pinpoint hemorrhages for a flea bitten appearance.
Describe chronic transplant rejection.
Describe transplant viral infections.
Rising creatinine levels, antibody mediated or cell mediated, changes to the glomerulus and like any chronic condition, interstitial fibrosis and tubular atrophy
Viral infections often happen in the transplanted organ due to immunosuppression (polyomavirus, CMV, adenovirus), visible as viral inclusions in tubular epithelial cells
Describe hyperacute transplant rejection.
Describe acute transplant rejection.
Pre-formed antibodies exist in the patient prior to the transplant and kill the kidney in minutes to hours (cyanotic with no urine output) meaning you must remove it and find a better match
Appears when serum creatinine levels gradually rise, usually mediated by T cells (acute cell mediated rejection) or when antibodies are produced after transplantation (acute antibody mediated rejection). Treat this with immunosuppressants. Causes vascular inflammation or tubular inflammation.
Describe the role of multiple myeloma on renal disease.
Describe light chain deposition disease.
Multiple Myeloma can also cause _______ to occur.
MM secretes monoclonal IG light chains that create large tubular casts causing inflammation (called cast nephropathy)
Unlike in cast nephropathy, the light chains deposit around the nephron (glomerular BM and mesangium) instead of within the tubules
Amyloidosis
Microscopically, how do you tell if something is a drug related interstitial nephritis?
Name the three forms of urate nephropathy.
Tons of pinkish / reddish eosinophils
Acute uric acid neohropathy (uric acid crystallizes in tubules with acidic pH in collecting ducts** and occurs with lots of cell turnover in tumor lysis syndrome)
Chronic urate nephropathy (monosodium urate crystals deposit in tubules, birefringent needle crystals)
Nephrolithiasis (kidney stones in patients with high uric acid levels)
Name some drugs that cause acute tubulointerstitial nephritis.
In 30% of acute tubulointerstitial nephritis cases, what is the cause?
Describe tubulointerstitial nephritis due to hypersensitivity to a drug.
Unlike other forms of acute tubulointerstitial nephritis, what cell types do drug reactions recruit?
Tubulointerstitial nephritis usually only affects what compartment?
Sulfonamides / penicillin / methicillin / ampicillin / rifampin / thiazides / NSAIDS / allopurinol
Unknown cause
Rash / not dose dependent / latent period / eosinophilia / elevated serum IgE, this is different than just a direct toxic injury
Eosinophils / lymphocytes*** (hence delay) / plasma cells
Tubulointerstitial compartment (only spreads to glomeruli if very severe)
Describe necrotizing papillitis.
What does ‘pyo’ mean?
Describe an acute pyelonephritis patient.
What will classically identify chronic pyelonephritis? It may cause _______ of the kidney, where they fill with protein.
May be seen in patients with diabetes, sickle cell, or obstruction of the tract which causes bilateral necrosis of papillary tips
Pus
Look sick, flank pain, fever, WBC cast, may have prior lower tract infection, oliguria, elevated creatinine
Irregular corticomedullary scars with blunted calyces (U shaped surface of kidney) and thin cortex full of dilated spaces, thyroidization
Describe pyelonephritis.
Very common, involves tubules / interstitium / renal pelvis, acutely caused by bacteria due to an ascending infection from the bladder, or chronically (some combination of bacteria with vesicouretal reflux (VUR) or obstruction). Can usually save the kidney with antibiotics, unless it has formed abscesses (due to neutrophil infiltration is acute). Microscopically, WBC casts (tubules packed full of neutrophils) and neutrophil infiltration in the parenchyma. The glomeruli tend to be spared. Fungal or Mycobacterial infections (TB) can create a granulomatous response (instead of an acute inflammatory response).
Differentiate between acute and chronic tubulointerstitial disease.
Acute = rapid onset / interstitial edema / leukocyte*** infiltration / tubular injury
Chronic = insidious onset / interstitial fibrosis / lymphocyte*** infiltration, tubular atrophy
What are the two general causes of tubular injury?
Name the most common cause of AKI. It is usually what?
What does ATN look like microscopically?
What can occur if the offending toxin is removed? What must be intact? Describe the appearance of cells that are recovering.
Ischemia / toxins (drugs or metabolism)
Acute tubular necrosis, reversible
Dying tubular epithelial cells, missing nuclei, epithelial casts, sloughed off cells, ruptured basement membrane, epithelial cells all packed together or not connected very well
Cell recovery, basement membrane, hyperchromatic / enlarged nuclei / mitosis
Very invasive UTIs will have treatments modified how? What drug do you give them?
What is the most effective prostatitis drug? Why might you contraindicate quinolones?
Most uncomplicated patients (like cystitis) get better how quickly? What about more invasive infections (pyelonephritis or prostatitis)? What do you order if they still don’t get better?
25% of pregnant women with UTI, who are not treated, develop what?
Longer treatments, quinolones (invasive infections require it despite resistance)
Quinolones, birth defects / expensive / interactions
1 day, 48-72 hours, CT scan
Pyelonephritis (so please treat them)
Describe some factors for complicated cystitis?
How do you treat an asymptomatic UTI? What three exceptions?
What drug treats them?
Why do you only use fluiroquinolones as a last resort?
Indwelling catheter, elderly, men, pregnancy, recent antibiotics, diabetes, immunosuppression
You don’t treat them, unless they have diabetes / pregnancy / immunocompromised
Nitrofurantoin (good for the bladder but not good for the kidneys), trimethoprim and fosfomycin (lower efficacy may not solve pyelonephritis)
E. coli are becoming resistant to it
If symptomatic, what diagnoses a UTI?
If asymptomatic, What diagnoses a UTI?
If symptomatic and midstream clean catch, what level may indicate UTI?
What about suprapubic aspiration (indwelling catheter)?
Over 10^5 CFU / ml
Two consecutive specimens with over 10^5 CFU / ml
Above 10^2 CFU / ml
Above 10^2 CFU / ml
Cystitis causes _____, _______ pain, ______ urine and the presence of what two things?
Acute pyelonephritis has a _____ onset of symptoms, including _____, ____, _____, and _________ tenderness. You can have a ______ cast, and it responds to therapy when?
What is the daily risk of catheter infection? How many catheterized patients develop a UTI? What are the most common pathogens? Always make sure the catheter collection bag is where? What will solve a catheter related UTI?
Dysuria, suprapubic, cloudy, WBCs and bacteria
Rapid, fever, nausea, vomiting, CVA, WBC, 48-72 hours
3-5 percent, 10-15%, E. coli, proteus, pseudomonas, below the level of the bladder (or else urine flows wrong way), remove the catheter
Loss of what bacteria can allow E. coli urinary tract colonization?
Name two urine characteristics that prohibit bacterial growth.
Why does drinking water decrease UTI?
30% of women with symptomatic cystitis do not show what? This indicates what as a potential etiology?
Typically urethritis lacks _____, has a _____ onset of symptoms, and has no ______ pain.
Lactobacilli
High osmolarity, high urea concentration
Flushed out the tract
No growth on cultures, STDs (don’t grow on culture easily)
Hematuria, gradual, suprapubic
Describe type 1 pili.
Describe type P pili.
What bacterial enzyme splits urea? What does it do? This _______ the urine and forms ______. What does it form in the renal pelvis?
Women with what blood-type are at increased risk for UTI?
Type 1 pili occur in most infectious bacteria, bind macrophages and inflammatory cells to evade immune system
Type P pili have a Pap G adhesion molecule on their tip, bind to oligosaccharides found in patients with P RBC antigens (thus patients with P antigens on their blood cells are prone to severe infections)
Urease, splits urea into ammonia and CO2, alkalinizes, stones, staghorn caliculi
P blood type
What term means high pressure urine going the wrong way?
Describe some bacterial virulence factors that inhibit or evade the immune system?
What specific E. coli serogroups have particularly effective virulence factors and can therefore infect the urinary tract easily?
Describe the function of exotoxin (like alphahemolysin).
What do bacterial fimbriae bind?
Vesicourethral reflux
Exotoxins, endotoxins, capsule polysaccharides (K antigen)
Serogroups O, K, H
It lyses RBCs to release iron, which siderophores (a type of protein) bind to and carry back to the organism
P antigen (this fimbriae and P pili bind the P antigen)
Why is the female urethra prone to gram negative colonization?
What increases risk of UTI in males?
20%-30% of asymptomatic bacteruria develop what in whom?
Anything that impedes what can cause infection? This back flow can also cause what condition?
Describe factors that impair bladder innervation and cause infections?
Proximity to anus and termination beneath labia
Age over 50, prostatic hypertrophy, rectal intercourse
Pyelonephritis (more serious), pregnant women
Urine flow (tumor, BPH, stones), hydronephrosis (and also papillary necrosis)
Spinal cord injury / multiple sclerosis / diabetic neuropathy
Most UTI infectious agents are what? Which one is most prevalent and how? Name some others.
Which gram positive organism is most common in UTIs? Who gets this?
What gram positive bacteria indicates recent surgical procedures?
What STI related organisms cause UTIs?
50% of UTIs involve what type of infection? 40% involve what?
Gram negative, E. coli (80% of acute infections) from anus, proteus, klebsiella, enterobacter, serratia, pseudomonas
Staphylococcus saprophyticus, young women
Staphylococci aureus
Chlamydia, neisseria, HSV
Cystitis (bladder infection), urethra
Name two acute lower tract infections. Are these invasive?
Name three upper tract infections. Are these invasive?
What is urethritis? What is cystitis? What is prostatitis?
Differentiate pyelonephritis from renal abscess.
What increases the occurrence of UTIs?
Urethritis and cystitis, no
Pyelonephritis, prostatitis, intra-renal abscesses, yes
Urethral infection (common with STDs), bladder infection (common in women), prostate infection
Pyelonephritis is a kidney infection without an abscess, whereas renal abscess is a kidney infection with an abscess
Age, sexual activity, female (25 times more likely)
Describe three dichotomous ways of classifying UTIs.
What does invasiveness determine?
Describe some non-invasive signs.
Describe some invasive signs.
Symptomatic versus asymptomatic, upper versus lower, mucosal (non-invasive) versus invasive (spreads to the parenchyma such as in the kidney or prostate)
Length of treatment (and possibly that you use quinolones)
Irritation (dysuria and frequency) without systemic symptoms (fever, flank pain, myalgia)
Irritation AND systemic symptoms
Describe three congenital penile abnormalities.
Describe condyloma acuminatum (genital warts)
Hypospadia (abnormal ventral opening), epispadia (abnormal dorsal opening), phimosis (precupice orifice too small for normal retraction)
Penile tumor by HPV 6 and 11, one or more papillary lesions (fibrovascular core), edges tumors dent like knuckles, HPV shrinks up the nucleus and makes a clear space around the nucleus (raisinoid) (Condo 611, sounds like knuckle)
Describe three types of carcinoma in situ of the penis.
First CIS is Bowen’s disease, caused by high risk HPV 16 (also causes oropharyngeal carcinoma), often age over 35, solitary gray or white plaque, will progress to an invasive carcinoma, microscopically will see dyskeratosis (keratin forms inside of cells too early hence gray white plaques), smooth round contour doesn’t breach the basement membrane.
Second CIS is bowenoid papulosis, high risk HPV 16 (like Bowen’s disease), younger males, red brown color, never progresses to invasive carcinoma, it eventually regresses (not as bad as Bowens disease)
Third is erythroplasia of Queyrat, histologically the same as Bowen’s disease, but shiny red or velvety plaques.
Describe squamous cell carcinoma of the penis.
Describe the prostate anatomy.
Usually on the glans or shaft, circumcision protects against carcinoma, most often occurs in uncircumcised smokers, associated with HPV 16 and 18, may be papillary or flat, want to make sure lymph nodes are not involved, can remove the penis.
Three zones: PZ peripheral zone (where most cancers occur), TZ transitional zone (some cancers occur), CZ central zone (surrounds prostatic urethra). A tubuloalveolar gland, two cell layer lining (basal layer with secretory cells), pink muscle fibers between glands
