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CPRII Exam 2 > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

What is the Henderson hasslebach equation

A

PH= 6.1 + log ([HCO3]/[pCO x 0.3])

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2
Q

What are the ranges for academia and alkalemia

A

<7.35 - acidemia

> 7.45 - alkalemia

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3
Q

What indicates a respiratory vs metabolic acidosis

A

Metabolic: HCO3 <20
Respiratory: pCO2 > 45

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4
Q

What differentiates a metabolic vs respiratory alkalosis

A

Metabolic: HCO3 > 30
Respiratory: pCO2 <35

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5
Q

What are some causes of acidosis

A

DKA, lactic acidosis, ingestion of ethylene glycol, methanol, propylene glycol, salicylates; loss of bicarbonate (diarrhea), AKI or chronic kidney dz

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6
Q

What conditions cause a normal anion gap metabolic acidosis

A

Diarrhea, ileal loop, renal tubular acidosis, carbonic anhydrase inhibitor, post hypocapnia

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7
Q

What causes a high anion gap metabolic acidosis

A

-salicylates, methanol, paraldehye, ethylene glycol, ketoacidosis, EtOH, lactic acidosis uremia

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8
Q

What are sx of acidosis

A

Flu - like; tachypnea and tachycardia (catecholamine release), pulm edema, increased serum glucose

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9
Q

What is a normal anion gap

A

8-12; its positive because you dont measure albumin

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10
Q

What is the compensation formula for metabolic acidosis

A

PCO2 = (1.5 x [HCO3]) + 8 (+/- 2) : if PCO2 doesn’t match then likely mixed

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11
Q

What does MUD PILES stand for

A
  • Methanol/metformin
  • Uremia
  • DKA
  • Paraldehyde/propylene glycol, phenformin
  • Isoniazid/iron toxicity
  • lactic acidosis *includes cyanide and CO poisoning, seizures, sepsis an ischemia
  • ethanol/ethylene glycol
  • salicylates
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12
Q

What are some causes of rhabdomyolysis

A

Seizure, extreme exercise, heat stroke, malignant hyperthermia, trauma, crush injury, immobilization, compartment syndrome; statins, SSRI, Cocaine, creatine, alcohol, toluene, CO, quail poisoning, mushroom poisoning; hypokalemia, hypophasphtema, influenza

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13
Q

What are the signs and sx of rhabdomyolysis

A

Decreased urine output, reddish brown color (myoglobin), heme + but no RBCs, positive protein, granular casts on micro; elevated CK, hyperkalemia, hypocalcemia, hyperphosphatemia

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14
Q

How does DKA occur

A

Intracellular hypoglycemia activates fatty acid degredation which lead to a large amount of ketones

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15
Q

Why do people with DKA start vomiting

A

Compensatory mechanism (drives towards alkalosis)

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16
Q

What does binge drinking do to insulin levels

A

Decreases them

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17
Q

What is ethylene glycol

A

Found in anti-freeze ; metabolized by alcohol DH to glycolic aid an then to oxalic acid; increased NADH levels encourage formation of lactic acid; *presents with intoxication, low BAC level, and HAGMA without ketones, calcium oxalate crystals in urine that fluoresce under wood lamps

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18
Q

What is characteristic of methanol poisoning

A

Blurry vision

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19
Q

How does salicylate toxicity present

A

Tachypnea (induces a respiratory alkalosis), tinnitus, agitation, seizures, coma, *salicylic acid contributes very little to acid load

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20
Q

How does renal failure lead to a high anion gap

A

Accumulation of sulfate, phosphate and other anions

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21
Q

Is acidosis common in chronic kidney dz

A

No* buffered by other organs as well as dietary changes and dialysis help prevent this

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22
Q

What are the alpha 1 receptor antagonists use to treat BPH

A

Terazosin, doxazosin, tamsulosin, silodosin, alfuzosin

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23
Q

What do the alpha 1 antagonists do to treat BPH

A

Relax m tone; *rapid relief of sx (days)

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24
Q

What does activation of each of the subsets of the alpha 1 receptors do

A

Alpha 1A: m contraction -> bladder outlet obstruction

Alpha 1D: detrusor instability

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25
Q

What do alpha 1 antagonists compete with

A

NE

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26
Q

Which alpha antagonists are not uroselective

A

Terazosin and doxazosin

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27
Q

What are the side effects of terazosin and doxazosin

A

Postural hypotension, dizziness, fatigue

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28
Q

What receptors are tamsulosin and silodosin specific or

A

Alpha 1A and alpha 1D

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29
Q

What are the side effects of tamsulosin an silodosin

A

Reduced ejaculation; IFIS (floppy iris syndrome)

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30
Q

Is alfuzosin specific for certain alpha 1 Receptors

A

No; but it is uroselective

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31
Q

What are the side effects of alfuzosin

A

QT prolongation

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32
Q

What drug interactions do all alpha 1 antagonists have

A

interact with PDE-5 inhibitors (sildenafil and vardenafil)

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33
Q

Which alpha 1 antagonists are metabolized by CYP 3A4

A

Tamsulosin, silodosin, alfuzosin

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34
Q

When should you avoid administration of alfuzosin

A

Hepatic impairment

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35
Q

When should you take alfuzosin

A

Immediately after same meal every day

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36
Q

What are the steroid 5alpha reductase inhibitors

A

Finasteride and dutasteride

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37
Q

What do the steroid 5alpha reductase inhibitors do

A

Prevent enlargement of and shrinks prostate; *delayed action - 3-6 months

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38
Q

What does a hyperplastic prostate have elevated levels of

A

SAR 2

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39
Q

Which steroid 5 alpha reductase inhibitor is specific

A

Finasteride (SAR-2); dunastride is a DUal inhibitor SAR 1 and 2

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40
Q

What is the effect of 5alpha reductase inhibitors on PSA

A

Decreases it

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41
Q

Which 5 alpha reductase inhibitor is more efficient at decreasing SERUM DHT

A

Dutasteride

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42
Q

What are the side effects of finasteride and dutasteride

A

ED, gynecomastia, depressed libido, ejatulation disturbances

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43
Q

Do the 5 alpha reductase inhibitors have drug interactions

A

No; but use caution with liver abnormalities by hepatic CYP3A

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44
Q

When do you use combination therapy for BPH

A

Severe sx of BPH, known to have large prostate, no response from monotherapy

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45
Q

What is tadalafil

A

PDE-5 inhibitor used to treat BPH an ED

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46
Q

What are the risk factors for ED

A

Obesity, smoking, stress, CV dz, adverse drug effect (diuretics, SSRI)

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47
Q

What are people with extrosphy of the bladder at risk for

A

Colonic glandular metaplasia and infections; adenocarcinoma

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48
Q

What are urachal cysts lined by

A

Either urothelium or metaplastic glandular epithelium

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49
Q

What kind of cancer can arise from urachal cysts

A

Carcinomas

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50
Q

What is the morphology of cystitis

A

Acute: hyperemia and neutrophil infiltrate *patients receiving cytotoxic antitumor drugs my developer hemorrhagic cystitis (adenovirus also causes this)

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51
Q

What is follicular cystitis

A

Presence of lymphoid follicle within the bladder mucosa

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52
Q

What is interstitial cystitis

A

Aka chronic pelvic pain syndrome; women; intermittent Supra public pain, urinary frequency, urgency, hematuria and dysuria, and cystoscope findings of fissures nd punctuate hemorrhages in the bladder mucosa; some are assoc with chronic mucosal ulcers (hunger ulcers) *increase mast cells is characteristic; r/o CIS

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53
Q

What is malakoplakia

A

Chronic inflammatory reaction that stems from acquired defects in phagocyte function; arises in setting of chronic bacterial infection occurs more in immunosuppressed transplant recipients

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54
Q

What is the morphology of malakoplakia

A

Soft yellow raised mucosal plaques filled with foamy macrophages that have abundant granular cytoplasm; *michaelis-Gutmann bodies present within macrophages (mineralized oncrtions from calcium in lysosomes)

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55
Q

What is polyploid cystitis

A

Inflammatory lesion resulting from irritation of the bladder urotheliumis thrown into broad bulbous polyploid projections

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56
Q

What is cystitis glandularis/cystica

A

Nests of urothelium (brunn nests) grown downward into lamina propria; epithelial cells in the center undergo metaplasia to cuboidal or columnar (glandularis) or retract to produce cystic spaces lined by flattened urothelium (cystica)

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57
Q

What is a nephrogenic adenoma

A

Unusual lesion that results from implantation of shed renal tubular cells at sits of injured urothelium; this tissue can be replaced by cuboidal epithelium whih can assume a papillary growth pattern

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58
Q

What are the precursor lesions to urothelial carcinoma

A

Noninvasive papillary tumors (most common) and flat noninvasive urothelial carcinoma

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59
Q

Invasion of what worsens the prognosis of bladder cancer

A

Muscularis propria

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60
Q

Is carcinoma of the bladder more common in men or women

A

Men

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61
Q

What are risk factors for bladder carcinoma

A
  • smoking
  • exposure to Aryl amines
  • schisto haematobium (but mostly squamous)
  • long term use of analgesics
  • heavy long term exposure to cyclophosphamide (immunosuppressant) induces hemorrhagic cystitis
  • irradiation
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62
Q

What mutations are seen in bladder cancer

A
  • GOF of *FGFR3 (found in noninvasive low-grade papillary carcinomas)
  • LOF in TP53 and RB (high grade and muscle invasive tumors)
  • *HRAS activation (low grade noninvasive)
  • =exclusive in bladder cancer
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63
Q

Losses of what chrom are common in bladder tumors

A

9; early events - first lose FGFR3, RAS and chrom 9 then lose TP53 and or RB

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64
Q

What is the morphology of papillary lesions of the bladder

A

Red, elevated; multiple tumors often present

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65
Q

What is the morphology of bladder papillomas

A

Often present in younger patients; single; attached by a stalk - exophytic; histo identical to urothelium; recurrences and progression rare; inverted papillomas are benign insisting o rods of urothelium that extend into the lamina propria

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66
Q

What are phosphodisterase inhibitors (PDE-5 inhibitors)

A

Sildenafil; competitive inhibitors

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67
Q

Which PDE-5 inhibitor has the fastest onset of action

A

Avanafil

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68
Q

Which PDE-5 inhibitors has the longest duration of action

A

Tadalafil (36 hrs)

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69
Q

Which PDE-5 inhibitors have to be taken on an empty stomach

A

Sildenafil an vardenafil

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70
Q

Which PDE-5 inhibitor has the longest half life

A

Tadalafil

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71
Q

What are the side effects of sildenafil, vardenafil, avanafil

A

Blue vision and blurred vision

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72
Q

What are the side effects of tadalafil

A

Back pain, myalgia, limb pain

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73
Q

What are the contraindications for PDE-5 inhibitors

A

Organic nitrates (extreme hypotension);

  • specific to vardenafil: patient needs to be hemodynamically stable
  • specific to tadalafil: when used or BPH, concurrent alpha 1 blockers not recommended
  • specific to sildenafil: concurrent alpha blockers initiated at lowest dose
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74
Q

What are the second line ED therapies

A

Vacuum erection devices and penile injections with alprostadil (prostaglandin E1)

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75
Q

How does alprostadil work

A

Increased cAMP, decreased iCa2+, smooth m relaxation and eretion

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76
Q

What are the side effects of alprostadil

A

Prolonged erection (priapism) *medial emergency -> can result in permanent corporal fibrosis and ED; tx with sympathomimetic (phenlephrine) and aspiration

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77
Q

What is pagetoid spread

A

Scattered malignant cells in otherwise normal epithelium

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78
Q

What are mixed urothelial carcinomas with areas of SCC

A

More frequent than pure SCC of the bladder; typically invasive, fungating tumors or are ulcerative and infiltraive

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79
Q

What is a good screening method for CIS

A

FISH of urine samples for aneuploidy of chrom 3,7,17, and 9p

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80
Q

What do patients at high risk of recurrence or progression (CIS, papillary high grade tumors, Multifocal or LP invasion) get for treatment

A

Intravesical instillation of attenuated Mycobacterium Boris called bacillus calmette-guerin-> elicits inflammatory response that kills tumor

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81
Q

What is radical cystectomy reserved for

A

Tumors invading muscularis propria, CIS or high grade papillary cancer refractory to BCG, CIS extending into prostatic urethra and prostatic ducts (BCG cant reach)

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82
Q

What is the most common benign mesenchymal tumor of the bladder

A

Leiomyoma

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83
Q

What is the most common sarcoma in infancy or childhood

A

Embryonal rhabdomyosarcoma can manifest as polyploid grape like mass called a sarcoma botryoides

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84
Q

What is the most common sarcoma in the bladder in adults

A

Leiomyosarcoma

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85
Q

What are the most common causes of obstruction of the bladder outlet

A

Males: prostate enlargement
Females: cystocele

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86
Q

What an happen secondary to BPH

A

Hypertrophy and trabeculation of bladder wall

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87
Q

What is an example of non infectious urethritis

A

Reactive arthritis

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88
Q

What is a urethral caruncle

A

Inflammatory lesion that presents as a small red painful mass at the external urethral meatus usually in older females; consists of inflamed granulation tissue covered by intact but extremely friable mucosa which can ulcerate and bleed *surgical excision

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89
Q

What are the benign tumors of the urethra

A

squamous and urothelial papillomas, inverted urothelial papillomas, condylomas

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90
Q

What is primary carcinoma of the urethra

A
  • proximal urethra: analogous to those occurring within later
  • distal: SCC
  • adenocarcinomas are rare but when they do occur, occur more often in women
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91
Q

What is the difference between epi and hypospadias

A

Epi is on dorsal side; hypo is on ventral

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92
Q

What are complications of hypospadias/epispadias

A

UTI, infertility

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93
Q

What is phimosis

A

When orifice of prepuce is too small to permit its normal retraction; frequently the result of repeated infection; favors development of secondary infections and possibly carcinoma

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94
Q

What is balanoposhitis

A

Infection of glans and prepuce; caused by candida, aerobic bacteria, gardnerella, and pyogenic bacteria; most cases occur cause of poor local hygiene in uncircumcised males -> accumulate smegma

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95
Q

What is the morphology of condylomata acuminata

A

Single or multiple sessile or pedunculated red papillary excrescences; superficial hyperkeratosis and thickening of underlying epidermis (acanthosis); no dysplasia; koilocytosis (vacuolization of squamous cells)

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96
Q

What is peyronie dz

A

Results in fibrous bands involving corpus cavernousum; lesions result in penile curvature and pain during intercourse

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97
Q

Which lesions of the male external genitalia display CIS

A

Bowen dz and bowenoid papulosis; strong association with infection by HPV type 16

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98
Q

What is Bowen dz

A

Occurs in men and women, usually > 35; in me: involves skin of shaft and scrotum; appears as solitary thickened gray-white opaque plaque; can manifest on the glans and prepuce s single or multiple shiny red velvety plaques histo: epidermis is hyperproliferative, dysplastic can transform to SCC

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99
Q

What is bowenoid papulosis

A

Occurs in sexually active adults; distinguished from Bowen dz by younger age of affected patients and presentation as multiple reddish brown papular lesions; never develops into invasive carcinoma

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100
Q

What confers protection against SCC of penis

A

Circumcision (rare in Jews and Muslim)

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101
Q

What increases risk of SCC of penis

A

HPV and smoking

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102
Q

What is an uncomplicated UTI

A

Nonpregnant outpatient women without an atomic abnormalities or instrumentation of urinary tract

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103
Q

What is a complicated UTI

A

Urinary obstruction, urinary retention cause by neuro dz, immunosuppression, renal failure, renal transplantation, pregnancy, foreign bodies (calculus, indwelling catheters)

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104
Q

What makes up the biofilm or UPEC

A

*type I pile, antigen 43, curli

105
Q

What makes up the biofilm for proteus

A

Produces urease; calcium crystals an magnesium ammonium phosphate precipitates; crystalline biofilm

106
Q

What makes up the pseudomonas biofilm

A

Micro colony formation by changing hyrophobicity of bacteria surface; lectins and rhamnolipids

107
Q

What makes up the biofilm of e.fecalis

A

Fibrinogen

108
Q

What are the first line treatments for uncomplicated cystitis

A

Nitrofurnantoin and fosfomycin; also TMP-SMX (trimethoprim-sulfamethoxazole)

109
Q

What bacteria are resistant too nitrofurantoin

A

Pseudomonas and proteus

110
Q

What is the pharmokinetics of nitrofurantoin

A

Metabolized and excreted so quickly that dont have systemic abx actions

111
Q

What are the adverse effects of nitrofurantoin

A

Antagonizes nlidixic acid (quinolone abx)

112
Q

What are the contraindications for nitrofurantoin

A

G6PDH deficiency

113
Q

What is the MOA of fosfomycin

A

Cell wall synthesis inhibitor; inhibits enolpyruvate transferase by binding to cysteine residue of active site and blocking addition of phosphoenolpyruvate to UDP-N-acetyleglucosamine

114
Q

How is resistance to fosfomycin developed

A

Inadequate transport of drug into cell

115
Q

What form is fosfomycin given in

A

Only oral; poor bioavailability

116
Q

When should nitrofurantoin and fosfomycin not be taken

A

If suspicion of early Pyelonephritis (does not achieve adequate levels in kidneys)

117
Q

What are the second line abx for cystitis

A

Oral beta lactams:

  • amoxicillin: aminopenicillin
  • cefpodoxime: 3rdd gen cephalosporin
  • cefdinir: 3rd gen cephalosporin
  • cefadroxil: 1st gen cephalosporin
  • less effective than fluoroquinolones but have less side effects so are second line
118
Q

What are the third line agents for cystitis

A

Fluoroquinolones: ciprofloxacin, levofloxacin, ofloxacin

119
Q

What are the adverse effects of fluoroquinolones

A

Tendinitis and tendon rupture, peripheral neuropathy, CNS effects
*effects outweigh benefits in treating uncomplicated cystitis

120
Q

What should you give if there is resistance to cystitis treatment

A

Ertapenem: good activity against gram neg, pos, and anaerobes but is inactive against pseudomonas

121
Q

According to Dr. Sheehy does cystitis present with a fever

A

No

122
Q

What are the first line agents for pyelonephritis

A

Fluoroquinolones: ciprofloxacin or levofloxacin

  • if severe pyelonephritis or risk factors for resistance -> administer with parenteral broad spectrum abx until susceptibility data is available (ceftriaxone or aminoglycosides - gentamicin and tobramycin)
123
Q

What are the aminoglycosides active against

A

Aerobic gram - and pseudomonas

124
Q

What is the MOA of aminoglycosides

A

Irreversible protein synthesis inhibitor - binds to 30S ribosome SU -> production of nonfunctional proteins

125
Q

What are the adverse effects of aminoglycosides

A

Eighth CN toxicity, renal toxicity, NMJ blockade

126
Q

What are the second line agents for pyelonephritis

A

TMP-SMX, oral beta lactams (amoxicillin, cefpodoxime, cefdinir, cefadroxil), if patient cant tolerate these agents -> aztreonam
*used in cases of fluoroquinolone hypersensitivity or resistance

127
Q

How is aztreonam administered

A

IV

128
Q

What are the adverse affects of aztreonam

A

Neutropenia, pain at injection site

129
Q

What do you us for complicated cystitis

A

Ciprofloxacin or levofloxacin

130
Q

What do you use for complicated pyelonephritis

A
  • mild: ceftriaxone, ciprofloxacin, levofloxacin or aztreonam
  • severe: beta lactam + beta lactamase inhibitor or a carbapenem
131
Q

What does the presence of a gram postiive cocci on gram stain suggest for a case of cystitis

A

E faecalis or E faecium; to with ampicillin or amoxicillin

132
Q

What is phenazopyridine

A

Urinary analgesia; can cause significant nausea an colors the urine orange/red

133
Q

Which first line agents for complicated pyelonephritis cover pseudomonas

A

Ciprofloxacin and levofloxacin

134
Q

What are the agents used for severe complicated pyelonephritis

A
  • cefepime
  • piperacillin + tazobactam
  • ceftolozane + tazobactam
  • ceftazidime + avibactam
  • meropenem
  • imipenem
  • doripenem
135
Q

What organisms do tazobactam and avibactam work well against

A

Good inhibitors of ambler class A beta lactamase: produced by staph, H. Influenzas, gonorrhea, salmonella, shigella, coli, klebsiella

*poor against class C: enterobacter, pseudomonas

136
Q

Are carbapenems resistant to beta lactamase

A

Yes

137
Q

What is the MOA of carbapenems

A

Inhibits transpeptidase

138
Q

Which carbapenem has the longes half life

A

Ertapenem

139
Q

What is the adverse effect of imipenem

A

Seizures

140
Q

What pathogen causes prostatitis most commonly

A

E coli

141
Q

What is the clinical presentation of prostatitis

A

Dysuria, urgency, Fever, pain; prostate is warm, firm, edematous

142
Q

What is the treatment for prostatitis

A

TMP-SMX, ciprofloxacin, levofloxacin

143
Q

How do you treat a recurrrent group A beta hemolytic strep infection

A

Repeat treatment should be with greater beta lactamase stability

  • penicillin G
  • cephalexin or cefadroxil (1st gen)
  • cefpodoxime or cefdinir (3rd gen)
  • amoxicillin or clindamycin
144
Q

What is the MOA of clindamycin

A

Binds 50s SU and inhibitors protein synthesis

145
Q

What is the morphology of SCC of the penis

A

Two types: papillary and flat

  • papillary forms cauliflower mass that fungates
  • flat: epithelial thickening accompanied by graying and fissuring
146
Q

What is verrucous carcinoma

A

Exophytic well differentiated variant of SCC that is locally invasive but rarely metastasizes

147
Q

What are the major lesions of the testis vs epididymis

A

Testis: tumor
Epididymis: inflammatory diseases

148
Q

What is synorchism

A

Fusion of testes

149
Q

What are the phase of descent of the testis

A
  • transbdominal: testis lie within lower abdomen; controlled by mulllerian inhibiting substance
  • inguinoscrotal phase: descend through inguinal canal to scrotal sac androgen dependent
150
Q

What is the most common site of undescended testis

A

Inguinal canal usually unilateral

151
Q

What is the morphology of cryptorchidism

A
  • arrested germ cell development associated with marked hyalinization and thickening of the BM of the spermatic tubules
  • leydig cells spared
  • small and firm
152
Q

What is orchiopexy

A

Placement of undescended testicle in the sac

153
Q

What is thought to cause cryptorchidism

A

Defect in testicular development and differentiation; not anatomy
-cancer can occur in contralateral testicle as swell

154
Q

What can cause testicular atrophy

A
  • progressive atherosclerotic narrowing of the blood supply in old age
  • end stage of inflammatory or orchitis
  • cryptorchidism
  • hypopituitarism
  • generalized malnutrition or cachexia
  • irradiation
  • prolonged administration of antiandrogens
  • exhaustion atrophy (following persistent stimulation by FSH)
155
Q

What infections affect the testis vs epididymis

A

Testis: syphilis
Epididymis: gonorrhea and tuberculosis

156
Q

What are the most common causes of epididymitis in diff age groups

A
  • childhood: gram - rods
  • younger than 35: chlamydia and gonorrhea
  • older than 35: E. coli and pseudomonas
157
Q

What is idiopathic granulomatous orchitis

A

Granuloma restricted to spermatic tubules; autoimmune cause suspected

158
Q

How does gonorrhea progress in males

A

Urethra -> prostate -> seminal vesicles -> epididymis (abscesses)

159
Q

When does mumps more commonly produce orchitis

A

Postpubertal

160
Q

How does syphilis affect the male GU tract

A

Gumma formation and diffuse interstitial inflammation that produces obliterative endarteritis associated its perivascular cuffs of lymphocytes and plasma cells

161
Q

What is the difference between neonatal and adult torsion

A

Adult: results from bilateral an atomic feet that leads to increased mobility of the testes (bell clapper abnormality) - fix this by orchiopexy

162
Q

What are the spermatic cord tumors

A
  • lipomas: common - involve proximal spermatic cord; usually just pulled fat from retroperitoneum by a hernia (not true neoplasm)
  • most common* - adenomatoid tumor; mesothelioma but NOT referred to as mesotheliomas; typically near upper pole of epididymis; benign; can be minimally invasive
  • most common paratesticular tumors are rhabdomyosaromas in children and liposarcomas in adults
163
Q

What is the difference between germ cell and sex cord tumors

A

Germ cell - malignant

Sex cord - tend to be benign

164
Q

What are the germ cell tumors divided into

A
  • seminomatous: seminoma and spermatocyticc seminoma

- nonseminomatous: embryonal carcinoma, yolk sac, choriocarcinoma

165
Q

What are the sex cord stromal tumors

A

Leydig cell or Sertoli cell tumor

166
Q

What population are germ cell tumors more common in

A

Whites

167
Q

What are testicular germ cell tumors associated with

A

Testicular dysgenesis syndrome (TDS): cryptorchidism, hypospadias, and poor sperm quality *increased by in utero exposure to pesticides and nonsteroidal estrogens

168
Q

What is klinefelter associated with an increase risk of

A

Mediastinal germ cell tumors but not testicular tumors

169
Q

What genetic factors have been linked to germ cell tumors

A

-KIT and BAK

170
Q

What is the precursor lesion for testicular germ cell tumors

A

Intratubular germ cell neoplasia (ITGCN)

171
Q

Which germ cell tumors do not typically arise from a precursor lesion

A
  • pediatric yolk sac tumors and tertomas

- adult spermatocytic seminomas

172
Q

What is the pathogenesis of germ cell tumors

A

Precursor lesion believed to occur in utero and stay dormant until puberty when it progresses; the precursor lesion cells retain xpresion of OCT3/4 and NANOG which are impt in maintenance of pluripotent stem cells; have reduplication of short arm of chrom 12 in the form of an isochrom (*always found in germ cell tumors)

173
Q

What is the equivalent tumor of a seminoma in the female

A

Dysgerminoma

174
Q

What do seminomas express.

A

Contain isochrome 12p and express OCT3/4 and NANOG

175
Q

What is the morphology of a seminoma

A

Sheets of uniform cells divided into poorly demarcated lobules by delicate fibrous septa containing lymphocytic infiltrate; large and round to polyhedral and has distinct cell membrane, clear o watery-appearing cytoplasm; large central nucleus with one or two prominent nuclei; stain positively for KIT, OCT4 and placental alkaline phosphatase (PLAP) 15% contain syncytiotrophoblasts (HCG elevated)

176
Q

What is spermatocytic seminoma

A

Typically affects older men; excellent prognosis; contain 3 cell populations: medium sized cells, smaller cells with a narrow rim of eosinophilic cytoplasm, and scattered. Giant cells; *lack lymphocytes, granulomas, syncytiotrophoblasta, extra-testicular sites of origin, admixture with other germ cell tumors and association with ITGCN

177
Q

What are the features of embryonal carcinoma

A
  • occur in 20-30 y/o age group
  • more aggressive than seminomas
  • smaller than seminomas
  • extension through tunica albuginea typically occurs
  • foci of hemorrhage or necrosis sen; histo: cells grow in alveolar or tubular pattens sometimes with papillary convolutions
  • markers: OCT3/4, PLAP, ***cyotokeratin and CD30 and negative for KIT (characteristic)
178
Q

What is a yolk sac tumor aka endodermal sinus tumor

A

Most common testicular tumor in infants and children up to 3 years; very good prognosis at this age; compose of lace-like (reticular) network of cuboidal or flattened cells; Schiller-Duvall bodies (consist of mesodermal core with central capillary and visceral and parietal layer of cells resembling primitive glomeruli) hyalin like globules in which alpha fetoprotein and alpha antitrypsin can be seen*

179
Q

What is fanconi syndrome

A

Dz of proximal renal tubular; filtered glucose, aa, Uric acid, phosphate, bicarbonate are not reabsorbed

180
Q

What are the clinical features of fanconi

A

Polyuria, polydipsia, hypovolemia, hypophosphatemic Ricketts (kids), osteomalacia (adults), growth failure, type 2 RTA, hypokalemia, hyperchloremia, hypophosphatemia, glycosuria (can also be caused by SGLT2 inhibitors)

181
Q

What are the causes of fanconi

A

Cystinosis, galactosemia, glycogen storage, tyrosinemia, Wilson’s, malignancy, multiple myeloma, nephrotic syndrome, renal transplant, heavy metals, meds (tenofovir, valproate, gentamicin)

182
Q

How do you tx fanconi

A

Replace substances wasted; use citrate to replace HCO3, phosphate, vit D, if genetic -> minimize intake of substance not handled properly

183
Q

What is the main difference between barter syndrome and gitelmann syndrome

A

Barttman: concentrating capacity and diluting capacity are reduced
Gitelmann: concentrating capacity is normal but diluting capacity is reduced

184
Q

What is classic barrters syndrome

A

Type 3 -> mutation in Cl channel in loop of henle

185
Q

What is the inheritance pattern of bartter

A

AR

186
Q

What is the presentation of barter syndrome

A

-neonatal form: polyhydramnios, polyuria/dipsia with hypercalcuria after birth
-classic form: no noticeable symptoms until school age; polyuria/dipsia, vomiting and growth retardation
Sx identical to those taking loop diuretics

187
Q

How do you tx barter syndrome

A

Increases in dietary sodium and potassium; potassium sparing diuretics to limit K loss; NSAIDs -> decreases production of PGE2 which helps the abnormalities seen in barter

188
Q

What are PE findings of barter

A

Normal to low BP, polyuria/dipsia, elevated plasma renin and aldosterone, hypokalemia, hyponatremia, hypocalcemia, hypomagnesmia, hypochloremic metabolic alkalosis, hyperglycemia, hyperuricemia, increased cholesterol *isotonic urine

189
Q

What is gitelmann syndrome

A

AR that affects the distal tubule; usually presents in late childhood more severe in females; patients usually have mutations in gene coding for thiazide sensitive Na-Cl cotransporter (NCCT); mimics chronic use of thiazide diuretics; may develop HTN at later age

190
Q

What is the presentation of gitelmann syndrome

A

Polyuria/dipsia, hypokalemia, hypercalcemia, hyponatremia, hypomgnesemia, hypochloremic metabolic alkalosis, hyperglycemia, hyperuricemia, incrased cholesterol; can dilute or concentration urine

191
Q

What is the tx for gitelmann syndrome

A

Taking in enough NaCl and providing supplementation of potassium and magnesium (will increase GI side effects so aim for stable hypokalemia and borderline hypomagnesemia) aldosterone antagonist can stabilize hypokalemia

192
Q

Is barter or gitelman more benign

A

Gitelman

193
Q

What is the defect in Liddle syndrome

A

ENaC channels dont degrade in principle cells; increased sodium reabsorption with potassium loss; AD

194
Q

What are the sx of liddle syndrome

A

(Pseudoldosteronism); severe HTN, low plasma renin activity, low aldosterone, metabolic alkalosis, hypokalemia

195
Q

What is pseudohypoaldosteronism

A

Caused by a failure of response to aldosterone leading to renal tubular acidosis and hyperkalemia; levels of aldosterone are actually elevated; therapy requires large amount of sodium

196
Q

What are the features of types I, II, and IV of RTA

A

Type I: decreased excretion of H+ and NH4; normal anion gap
Type II: loss of HCO3 b/c cant reabsorb it; normal anion gap hyperchloremia
Type IV: hypoaldosteronism; decreased excretion of NH4; hyperkalemia inhibits NH3 synthesis; normal anion gap

197
Q

What are the features of all RTAs

A

Acidemia, normal anion gap, normal serum creatinine, and NO diarrhea

198
Q

What is the most common RTA

A

Type IV; hyperkalemic*; plasma HCO3 is >17; urine pH is typically <5.5; common causes: diabetic neuropathy, harmonic interstitial nephritis, drugs: ACEI, ARB, heparin, NSAIDs, spironolactone

199
Q

What is the plasma K+ in RTA type I vs type I

A

Type I: low, but fixed with alkali therapy

type II: low, but worsened by alkali therapy

200
Q

What are some common causes of RTA type I

A

Autoimmune disorders, kidney transplant, hypercalcuria, sickle cell, cirrhosis, analgesic nephropathy

201
Q

What are the common causes of RTA type 2

A

Fanconi, in adults: multiple myeloma, drugs

202
Q

Where is the location of the deficit in each of the RTAs

A

Type I: distal
Type II: proximal
Type IV: adrenal

203
Q

Which RTA causes the most severe acidosis

A

Type I

204
Q

What are other presenting features of RTA I

A

Urinary stone formation b/c hypercalcuria with low urinary citrate and alkaline urine; bone demineralization

205
Q

How do you tx RTA I

A

Restoring normal growth and preventing kidney stones is goal; sodium bicarbonate or sodium citrate to treat acidosis; correction of low K, Ca and salt

206
Q

How do you tx RTA 2

A

Treat underlying cause; children with this disorder: give large doses of potassium citrate (oral alkali)

207
Q

How do you tx RTA 4

A

Therapy aimed at reducing potassium; low potassium diet and loop diuretic; alter drug doses

208
Q

What is the morphology of choriocarcinoma

A

Do not cause testicular enlargement; small palpable nodul; hemorrhage and necrosis extremely common; histo 2 cell types - syncytiotrophoblast(large multinucleated contain HCG) and cytotrophoblast (polygonal with clear cytoplasm row in cords or masses and have single nucleus)

209
Q

What does hemorrhage and necrosis with a teratoma usually indicate

A

Admixture with embryonal carcinoma and/or choriocarcinoma

210
Q

What is the importance of recognizing a non-germ cell malignancy arising in a teratoma

A

These secondary tumors are chemo resistant

211
Q

When are teratomas considered malignant

A

In postpubertal male

212
Q

Do you usually bx testicular masses

A

No because there is a risk of tumor spillage; the standard management of solid testicular mass is radical orchiectomy based on presumption of malignancy

213
Q

How do testicular tumors spread

A

Lymphatic - retroperitoneal para aortic nodes are first to be involved; hematogenous to lungs primarily

214
Q

What are the differences between seminomas and nonseminomatous germ cell tumors

A
  • seminomas tend to remain localized to the testis; NSGCTS spreads faster
  • Mets from seminomas involve LN; NSGCTs use hematagenous route
  • NSGCT - poorer prognosis
215
Q

What are the stages of testicular tumors

A

I: confined to testis, epididymis or spermatic cord
II: distant spread confined to retroperitoneal nodes below diaphragm
III: met outside the retroperitoneal nodes or above the diaphragm

216
Q

What does the elevation of lactate DH indicate

A

Mass of tumor cells; assesses tumor burden

217
Q

What tumor produces AFP

A

Yolk sac

218
Q

How can serum markers be used in testicular tumors

A

Elevation of AFP or HCG father orchiectomy indicates stage II dz; monitoring response to therapy

219
Q

What are the sx of leydig cell tumors

A

Testicular swelling, gynecomastia

220
Q

What is the morphology of leydig tumors

A

Large, polygonal, cytoplasm contains lipid droplets, lipofuscin, *crystalloids of reinke

221
Q

What are gonadoblastomas

A

Composed of germ cells and stromal elements

222
Q

What is the most common form of testicular neoplasm in men over 60

A

Non-Hodgkin lymphoma; most common is diffuse B cell lymphoma, Burkitt, and EBV positive extra nodal; * have high propensity for CNS involvement

223
Q

What is the tunica vaginalis

A

Mesothelial lined surface exterior to the testis that can accumulate fluid (hyrocele); rarely can develop mesothelioma; hematocele; chylocle - lymph (elephantiitis)

224
Q

Where do most prostatic hyperplasia occur

A

Transitional zone

225
Q

Where do most carcinomas of the prostate occur

A

Peripheral zone

226
Q

What causes acute bacterial prostatitis

A

Bacteria similar to those that cause UTI E. coli and staph; fever, chills, dysuria; on rectal exam, prostate is tender and boggy; dx via urine culture

227
Q

How do you dx chronic bacterial prostatitis

A

Leukocytosis in the prostatic secretions and positive bacterial cultures

228
Q

What is the most common form of prostatitis

A

Chronic abacterial prostatitis; no hx of UTI*; leukocytes in prostatic secretions but culture is negative

229
Q

What causes granulomatous prostatitis

A

Most common: instillation of BCG within the bladder for treatment of superficial bladder CA; requires no tx; can also be caused by rupture of prostatic ducts

230
Q

What are the syndromes that include wilms tumor

A
  • WAGR: wilms, aniridia, genital, retardation
  • denys-drags: gonadal and renal tumors
  • beckwith-wiedemann: non-WT1; IGF2
231
Q

What cells are hyperplastic in BPH

A

Stromal and epithelial lols

232
Q

Is there increased epithelial proliferation in BPH

A

No; postulated that it forms from lack of cell death

233
Q

What is the difference between type 1 and 2 5 alpha reductase

A

Type I: is in liver and skin

Type II: in prostate (stromal cells; not epithelial)

234
Q

What does DHT bind to

A

Nuclear androgen receptor in stromal and epithelial prostate cells; has a higher affinity than testosterone -> stimulates formation of FGF and TGF beta; increases proliferation of stromal cells and decreases death of epithelial cells

235
Q

What is the morphology of BPH

A

-early, just stromal cells; late predominantly epithelial; median lobe hypertrophy; nodules that contain mostly glands are yellow-pink an soft and exude milky white prostatic fluid; nodules that are composed of fibromusclar stroma are pale gray and tough and do not excrete fluid

236
Q

What can BPH cause downstream

A

Bladder hypertrophy and distention with urine retention; infection;

237
Q

How is BPH treated

A

Decreased fluid intake, moderating intake of alcohol and effeminate, timed voiding schedules; alpha blockers; 5 alpha reductase inhibitors; severe: transurethral resection of prostate

238
Q

What population does prostatic cancer most frequently occur in

A

Black

239
Q

What products prevent prostate cancer

A

Lyopenes (tomato’s), soy, vitamin D

240
Q

What does the X-linked AR gene contain

A

CAG repeats; AR with shortest CAG repeats have highest sensitivity to androgens - found in AA

241
Q

How do tumors evade antiandrogen treatment

A

Acquiring hypersensitivity to low androgen levels (AR gene amplification), ligand-independent AR activation, mutations in AR that allow it to be activated by non-androgen ligands; increased PI3K/AKT signaling (loss of PTEN)

242
Q

What genes are associated with prostate cancer

A

BRCA2, HOXB13 (familial)

  • chromosomal rearrangements that juxtapose the coding sequence for ETS family TF genes (ERG or ETV1) next to anyone regulated TMPRSS2 promoter -> leads to overexpression of ETS which makes normal epithelial cells more invasive
  • deletions and amplifications are more common; amplification of 8q24 containing MYC and deletions of PTEN; late stage: loss of TP53 and RB
  • hypermethylation of glutathione s transferase (GSTP1) - downregulates GSTP1 expression - prevents damage from carcinogens
243
Q

What is the precursor lesion to prostate cancer

A

Prostatic intraepithelial neoplasia (PIN) but not referred to as CIS

244
Q

What is the morphology of prostate cancer

A

Gritty and firm; local extension involves seminal vesicles and base of urinary bladder; Mets via LN to obturator nodes and para aortic node; hematogenous spread to bones (typically osteoblastic) - most common in lumbar spine, proximal femur, pelvic, thoracic spine and ribs; *outer basal cell layer that lines benign glands is absent (but is found in PIN); *histo features specific for prostate cancer: perineural invasion; use alpha methylacyl coenzyme A racemase (AMACR) as immuno marker

245
Q

What are the prognostic predictors for prostate cancer

A

Grade and stage

246
Q

What is the Gleason system

A

Grade I: most well differentiated tumors - grade 5: no glandular differentiation with tumor cells infiltration the stroma in cords, sheets and nests

247
Q

How is Gleason score calculated

A

Primary stage + secondary stage; if only one pattern, double it; if three pattens most common and highest grade adde

248
Q

What does each range of Gleason scores indicate

A

2-6:excellent prognosis

7-10: poor prognosis

249
Q

What are the stages of prostate cancer

A

T1: incidentally found
T2: organ confine
T3a and b: extra prostatic extention with and w/o seminal vesicle invasion, respectively
T4: direct invasion of contiguous organs
N0: no LN met
N1: met in LN

250
Q

What is needed to confirm the dx of prostate cancer

A

Trans rectal needle biopsy

251
Q

What form of PSA is more prominent in cancer vs BPH

A

BPH: free
Cancer: bound to alpha 1 antichymotyrpsin

252
Q

Which genes are biomarkers for prostate cancer

A

PCA3 (urine); combined with urine screening for TMPRSS2-ERG fusion may have increased sensitivity than PSA alone

253
Q

What is the most common tx for local prostate cancer

A

Radical prostatectomy

254
Q

How is advanced met carcinoma treated

A

Androgen deprivation by orchiectomy or administration o analogs of LHRH

255
Q

What is the prognosis for ductal adenocarcinoma of the prostate

A

Poor

256
Q

What is colloid carcinoma of the prostate

A

Carcinoma that reveals abundant mucinous secretions

257
Q

What is the most aggressive form of prostate cancer

A

Small cell (aka neuroendocrine)

258
Q

What is the most common cancer that secondarily involves the prostate

A

Urothelial cancer

CPRII Exam 2 (17 decks)

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