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Genitourinary Disorders Flashcards

1
Q

In males, what is the most common site for hyperplasia in the reprod tract?

A

Prostate

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2
Q

Will all men develop BPH?

A

Yes, some more severe than others.

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3
Q

What is BPH?

A

Gradual periurethral enlargement of prostate.

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4
Q

What are etiologic factors for BPH? (5)

A

Unclear. Ageing (altered T:E), ?genetic predisposition, ?race, ?diet

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5
Q

What is dihydrotestosterone (DHT)? What is this compound initially? What enzyme changes the compound into DHT?

A

DHT is a hormone that supports the structure and function of the prostate. Testosterone. 5a reductase changes T into DHT.

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6
Q

What hormone sensitizes the prostate to DHT?

A

Estrogen

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7
Q

What is the patho of BPH?

A

T:E ratio is altered - quantitative dec in T and relative inc in E - E sensitizes prostatic cells more so than before - prostatic cells more responsive to DHT - enlargement of prostate (hyperplasia) and hypertrophy of smooth muscle cells - hyperplasia of periurethral tissue - compresses urethra - impedes urine flow

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8
Q

Where does most of the change occur in BPH (what area of tissue) and if it continues to grow where will the growth progess?

A

Periurethral tissue but will progress peripherally and peripheral prostate tissue will be affected.

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9
Q

What compensatory mechanisms are there with BPH? Are these compensatory mechanisms helpful?

A

Bladder wall thickens (prevents bladder from bursting) and trabeculations and diverticuli (in pouchings in bladder wall increase bladder capacity). These compensatory mechanisms are not good and cause more issues than good.

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10
Q

What are complications of BPH (4)?

A

Renal calculi and UTI from urine stasis (because of increase bladder volume). Hydroureter (urine backs up into ureters creating a “fish hook”) and hydronephrosis (urine retention in kidney) d/t urine backing up into kidney from complete obstruction?

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11
Q

What are 4 manifestations of BPH?

A

Frequency, hesitancy, weak urine stream, and terminal/post-void dribbling.

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12
Q

How is BPH diagnosed (5)?

A

DRE, PSA (prostate-specific antigen, prostate secretes PSA, inc total PSA = inc prostate tissue), BUN, Creatnine, urinalysis (infection and hematuria)

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13
Q

What is PSA D, and PSA V? What do these show? What do you need to determine these values?

A

PSA D = density of prostate cells
PSA V = velocity of which prostate is enlarging.
Need US

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14
Q

What is often the treatment for BPH? 1st line treatment? What next if that doesn’t work? Next? Final treatment option?

A

Often no treatment. 1st line: alpha adrenergic antagonist (smooth muscle relaxes and facilitates voiding). Then add: 5a reductase inhibitor (decreases DHT). If severe enough combine both drugs. Surgery (transurethral resection of prostate TURP, laser prostatectomy)

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15
Q

Which cancer is the most common cancer in men? It is not aggressive with older men but when it occurs in younger men it is aggressive?

A

Prostate cancer.

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16
Q

What are risk factors for prostate cancer (5)?

A

age, diet, ethnicity, familial (1st and 2nd generation), androgens.

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17
Q

What is the most common type of prostate cancer? What is the patho for prostate cancer?

A

Adenocarcinoma. Peripheral prostate affected. Can be multicentric, no early manifestations (hard to diagnose), often has mets by diagnosis, manifestations commonly occur from mets and extension than the actual primary tumor, extends to seminal vesicle and bladder first. Then will mets to bones, lungs, liver.

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18
Q

What are 2 manifestations of prostate cancer?

A

Prostatitis (common), and late hip and back pain (indicating bone mets)

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19
Q

What 4 diagnostics are used to diagnose prostate cancer?

A

DRE, PSA, biopsy, transurethral US.

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20
Q

What is the treatment for non-aggressive and localized cancer? What is the treatment for aggressive cancer (2)?

A

Active surveillance (patient will most likely die from natural causes first before prostate CA). Radical prostatectomy (removing prostate and seminal vesicle) and radiation.

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21
Q

What are some etiologic factors for PID?

A

Polymicrobial (especially bacteria - E. coli), also chlamydia, staphylococci, streptococci, and gonorrhea.

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22
Q

What is the patho of PID? What manner does the infection spread?

A

MO enter the cervix (when dilated during menses) - impact the endometrium - impact the tubes. Ascending manner.

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23
Q

What enables bacteria to proliferate so quickly?

A

Sloughing of the endometrium as it provides nutritional material for bacteria.

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24
Q

What are complications of PID (4)?

A

Pelvic abcess in abdominal cavity leading to peritonitis. Sepsis, and infertility (scarring).

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25
Q

What are 6 manifestations of PID?

A

Lower abdominal pain, heavy purulent discharge, dyspareunia (painful sex), adenexal tenderness (near uterus), fever, leukocytosis.

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26
Q

What 4 ways is PID diagnosed?

A

Presentation (important), increase ESR (erythrocyte sedimentation rate - indicates inflm), increased CRP, exploratory surgery.

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27
Q

What 3 treatment methods are used for PID?

A

Multiple broad spectrum abx (90% success rate), evaluate and treat sexual partner, and surgery at times (abcesses).

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28
Q

Which is the most common type of female cancer affecting the reproductive system? Rarely seen in men?

A

Breast cancer.

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29
Q

What are 4 etiologic/risk factors for breast cancer?

A

Increased age, genetic predisposition, hereditary, hormonal factors (providing E for menopause, early menarche, late menopause, nulliparity - increased exposure to estrogen).

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30
Q

What genes are involved in the hereditary forms of breast cancer?

A

BRCA1 on Chromosome 17 and BRCA 2 on chromosome 13.

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31
Q

What are the 8 types of malignant breast cancers?

A

Ductal carcinoma in situ, infiltrating ductal carcinoma, infiltrating lobular carcinoma, medullary carcinoma, colloid carcinoma, tubular carcinoma, inflammatory breast CA, Paget’s disease.

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32
Q

Which form of malignant breast cancer is the most common?

A

Infiltrating ductal carcinoma (75%).

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33
Q

What are the characteristics of ductal carcinoma in situ (breast cancer)?

A

Non invasive because it is in situ. 20%, intraductal. Stage 0 means the tumor will become invasive if not dealt with.

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34
Q

What are the characteristics of an infiltrating ductal carcinoma (breast cancer)?

A

Most common. Ductal origin (solid, irregular mass), invasive (will invade into duct tissue), proximal mets to axillary lymph nodes, distal mets (liver, bone, and brain), malignant cells arise will destruct resident tissue and deposit collagen fibre in breast.

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35
Q

What are the characteristics of an infiltrating lobular carcinoma (breast cancer)?

A

10-15 %. arise in lobular epithelium, often multicentric and can be bilateral.

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36
Q

What are the characteristics of medullary carcinoma (breast cancer)?

A

Treated as infiltrating ductal carcinoma.

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37
Q

What are the characteristics of colloid carcinoma (breast cancer)?

A

Mucous producing CA cells, better prognosis, dec chance of mets.

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38
Q

What are the characteristics of tubular carcinoma (breast cancer)?

A

Good prognosis, dec chance of mets.

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39
Q

What are the characteristics of inflammatory breast CA?

A

CA cells spread to lymph node channels in skin of breast, manifestations are: edema, larger breast in diseased breast, and erythema of skin.

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40
Q

What are the characteristics of Paget’s disease (breast CA)?

A

Occurs in women over 50, manifestations are: scaly, erythematous, pruritic lesion of nipple. Often represents ducal carcinoma in situ of nipple.

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41
Q

What is the most common location for breast cancer to arise (quadrant)? What are 5 manifestations? Which manifestations are late?

A

UOQ. Fixed, irregular painless mass. Late: pain, discharge, retractions, edema.

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42
Q

How is breast cancer diagnosed? (5)

A

Mammography (screen), biopsy, E+P receptors (quantity of the receptors indicates if tumor relies on hormone to grow), CEA, patient.

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43
Q

In terms of breast cancer - what tumor markers are used for diagnosis? Where is this compound also found?

A

CEA (carcinoembryonic antigen) marker for breast CA, but not specific to. Also for colorectal CA. Is a protein present in breast tissue, excess CEA indicates excess cells. Fetal GIT.

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44
Q

How is breast cancer treated (4)?

A

Surgery, chemo, radiation, Hs.

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45
Q

When would hormones be used to treat breast cancer? What kinds of therapies can be used?

A

When E/P receptors are very high hormone therapy is used. Can use: tamoxifen (anti-E), E, androgen, and progestins. Can use the same hormone to down regulate receptors.

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46
Q

What is a lumpectomy?

A

Excise the tumor and surrounding tissue.

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47
Q

What is a quadrantectomy?

A

Removal of entire quadrant

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48
Q

What is a mastectomy?

A

Removal of entire breast.

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49
Q

It’s not how much of the breast that is affected by CA that determines prognosis but it is the ________________________ that determines prognosis.

A

Involvement of axillary nodes.

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50
Q

Which is the most lethal form of female reproductive CA? Why?

A

Ovarian because it is difficult to diagnose with no early signs, no suitable screen, advances silently and has mets by diagnosis in 75% of cases.

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51
Q

What are 4 etiologic/risk factors for ovarian cancer (include other factors)?

A

Ageing (cumulative exposure to potential carcinogens and ovulatory age - length of exposure to sex hormone), autosomal dominant, family history, other factors: nulliparity, infertility, dysmenorrhea.

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52
Q

What types of ovarian cancers are there (where do they develop)? What is the patho for ovarian cancer, one or both ovaries? Where can it extend to? Where can the malignant cells seed?

A

Epithelial (90%), germ cell, or stromal tumors. Malignancy is usually in one ovary, can spread/extend to: tubes, ovary, uterus and ligaments. Bowel surfaces, liver, and other organs. Puts pressure on adjacent organs and abdominal distention occurs.

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53
Q

What are some early, non-specific manifestations of ovarian CA? 4 others? Late manifestation?

A

GI disturbances (flatulence, bloating, abdominal discomfort). Abdominal distention (if mass is large on ovary), ascites and dyspnea (fluid shift d/t inflammation), urinary and bowel obstruction. Late: pelvic mass (usually 1st finding).

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54
Q

How is ovarian cancer diagnosed? Can this be used to determine extent and stage of tumor?

A

Laparotomy, yes.

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55
Q

What is the treatment for ovarian CA? What is done after surgery? What is done 6-24 months later… why is this done?

A

Aggressive treatment, surgery (remove ovary with malignancy, other ovary, uterus, tubes and omentum), chemo, then another laparotomy to determine need for further treatment.

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56
Q

Which is the most common pelvic CA in women?

A

Uterine (endometrial) cancer.

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57
Q

When does uterine CA usually affect women?

A

Age 55-65.

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58
Q

What are 3 etiologic factors for uterine cancer?

A

Hyperestrogenism, some unrelated to E, family history.

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59
Q

What are RF for uterine CA?

A

Obesity, ageing, pelvic radiation, DM, HTN .

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60
Q

Why is obesity a RF for uterine CA?

A
  1. adipose tissue stores E (the more adipose tissue the more E) and 2. adipose tissue synthesizes E.
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61
Q

What type of cancer is most common of uterine cancers? What is the patho for uterine CA? What are the characteristics of type 1? Type 2? Is type 1 or 2 more common?

A

Adenocarcinoma (as the endometrium is glandular and epithelial tissue). E - endometrial hyperplasia - pathological levels of E - hyperplasia - dysplasia - anaplasia. Type 1: E dependent, endometrial hyperplasia - dysplasia - anaplasia. Better prognosis. Type 2: Non E dependent, associated with atrophy of endometrium. Poor prognosis.

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62
Q

Where does the malignancy in uterine cancer eventually progress to? Is it slow or quick progressing? Will the cancer mets? Is there a reliable screen for this CA?

A

Deeper uterine layers (muscle) and vagina. Slow progressing. Yes. No reliable screen.

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63
Q

What are manifestations of uterine CA?

A

Painless vaginal bleeding (outside of period), others related to invasion and mets

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64
Q

How is uterine CA treated?

A

Surgery and radiation.

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65
Q

What are 4 et/RF for cervical CA?

A

HPV infection, early age sex/multiple sex partners, smoking, history for STDs.

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66
Q

Which strains of HPV cause 70% of cervical CA cases?

A

16 and 18

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67
Q

What is the patho for cervical CA? Origin? What is the initial change? Then what is next? Then? How many years are there between pre-CA and invasive stage?

A

Squamous cell. Initial dysplasia (pre-CA lesion), then carcinoma in situ (not yet invasive), then invasive CA. There are several years between pre-CA and invasive stage.

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68
Q

What is CIN? 1-3?

A

Cervical Intraepithelial Neoplasia (CIN). CIN 1: mild dysplasia (pre-CA), CIN 2: moderate dysplasia, CIN 3: severe dysplasia and carcinoma in situ (CA).

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69
Q

Will cervical cancer mets?

A

Yes.

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70
Q

How is cervical CA diagnosed?

A

PAP and colposcopy.

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71
Q

What are manifestations of cervical CA? (3)

A

Vaginal discharge and bleeding, metorrhagia, and increased frequency of menses.

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72
Q

How is cervical CA treated? Early? Invasive? Describe conisation.

A

Early: excision (CA in situ). Invasive: radiation and chemo. Conization is using cone-shaped instrument to remove cone-shaped CA lesions. Laser Sx (ablation), radial hysterectomy.

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73
Q

How does a UTI progress?

A

In ascending order (from urethra to kidneys)

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74
Q

What are 4 defences humans have to avoid UTIs?

A

Local immune response, mucin layer, prostatic fluid, periurethral flora.

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75
Q

What role does the mucin layer play in protecting against UTI? What about prostatic fluid? Periurethral flora?

A

Mucin layer = glycoprotein layer that prevents direct contact of urine with bladder lining), prostatic fluid has antimicrobial properties, and periurethral flora (in females) prevents foreign bacteria from establishing as there is excess normal flora that takes up space.

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76
Q

What are risk factors for a lower UTI?

A

Catheterization and obstruction (leading to stasis and losing “wash out” and causing reflux)

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77
Q

When do the manifestations of a lower UTI set in? What are 3 manifestations?

A

Acutely. Frequency (cannot empty bladder fully d/t inflammation reducing lumen size), dysuria, lower back pain.

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78
Q

How is a lower UTI diagnosed (3)?

A

Manifestations, urinalysis and C+S

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79
Q

How is a LUTI treated (2)?

A

Abx + underlying cause (ie. like BPH)

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80
Q

What is pyelonephritis? What structures are inflamed? Acute or chronic?

A

Upper UTI, renal pelvis + parenchyma. Acute + chronic.

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81
Q

What are the etiologic factors of PN?

A

Bacteria. E.coli most commonly.

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82
Q

What are the etiologic factors for LUTI?

A

Bacteria. Usually E.coli.

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83
Q

What are risk factors for PN (4)?

A

Same as LUTI, suppressed immunity, urinary reflux + DM.

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84
Q

What is the patho of PN? Chronic form?

A

Ascending infection + inflm (urethra - kidney), fibrosis + scar tissue (if acute form persists + this will be present in chronic form) then kidney function decreases
CHRONIC FORM: recurrent inflammation leads to obstruction or reflux leading to renal damage and eventually renal failure.

85
Q

What is a serious complication of pyelonephritis?

A

HTN

86
Q

What are manifestations of PN (6)? Do these manifestations take time to show up?

A

Lower back pain, fever, dysuria, frequency, urgency, pyuria.

87
Q

What is the treatment for PN?

A

Longer course of abx (10-14 days)

88
Q

What 5 types of categories of glomerular disease are there?

A

Nephrotic syndromes, nephritic syndromes, sediment disorders, rapidly progressive GN, chronic GN.

89
Q

What is nephrotic syndrome?

A

Increased glomerular permeability resulting in great fluid + protein loss.

90
Q

What is nephritic syndrome?

A

Reduced glomerular filtration resulting in fluid + electrolyte retention + nitrogenous waste retention.

91
Q

What is a sediment disorder? Can it be one or the other, or both?

A

Hematuria + proteinuria, can involve one or the other or both.

92
Q

What is GN?

A

Inflammation of the glomerulus.

93
Q

When does acute postinfectious (proliferative) GN (APIGN) occur?

A

Always precedes infections.

94
Q

Who does APGN affect most commonly? In the small amount of this age group of people, how common is it to form RF?

A

Mainly kids (95%), in adults 30% develop RF.

95
Q

Which infection precedes APGN? How many days post-infection does APGN occur?

A

Beta hemolytic (haemolyse RBC) strep infection in pharynx or skin. Occurs 7-12 days post-infection.

96
Q

What type of HS is APIGN? Walk me through the patho of this.

A

Type 3. IC traps + deposits in glomerulus leading to impeded glomerular filtration.

97
Q

What are the histologic/cytologic changes that occur in APIGN? (2) In the first histologic change what cells are there changes in?

A
  1. Hypercellularity (increase number of cells). 2. Glomerular enlargement. Leukocytes, mesangial + endothelial cells.
98
Q

What manifestations present in APIGN (5)? What causes some of the manifestations?

A

Oliguria followed by proteinuria and hematuria. Increase BUN, creatinine. Oliguria (impeded filtration d/t IC), proteinuria (inflammatory damage = holes), hematuria (damaged caps)

99
Q

What is a neurological complication of APIGN? Why?

A

Azotemia because nitrogenous wastes are retained due to decreased kindey fx + urine output

100
Q

What are two manifestations of APIGN? Why?

A

HTN + edema because of Na and H2O retention, as well as protein loss.

101
Q

How is APIGN treated? How long after it has set in place does recovery begin to occur? Are most cases self-limiting?

A

Symptomatic treatment (anti-inflammatory). 2 weeks. Most are self-limiting.

102
Q

Where can renal calculi occur? Who are these more prevalent in? Where do they form usually?

A

Anywhere in the urinary tract. Men. Kidney.

103
Q

What are 3 etiologic factors for renal calculi?

A

Structural changes in urinary tract (BPH), increased concentration of blood/urine components (hypertonic urine results in more content to precipitate out of urine), dietary + metabolic factors

104
Q

What does the kidney do that prevents crystallization of components in the urine? What is the patho for renal calculi?

A

Secretes 3 proteins. Increased solute concentration +/or urine stasis leads to components in urine to precipitate out, forming a nucleus and then crystallization.

105
Q

What are the 4 different types of renal calculi?

A

Calcium (oxalate + phosphate), magnesium ammonium phosphate (struvite), uric acid (urate), and cysteine.

106
Q

What are 4 manifestation of renal calculi? What are the 2 different types of pain a result from?

A

Severe renal colic: distended ureters/passing stone through urethra, non colicky pain: distension of renal pelvis + calyces. N+V, diaphoresis.

107
Q

How is renal calculi diagnosed (5)?

A

Pain (pattern), UC, CT, urinalysis, IVP (IV pyelogram - dye moves through UT to visualize stone).

108
Q

What are 4 treatment methods for renal calculi?

A

90% spread spontaneously (if less than 5mm in diameter), morphine + gravol, antispasmodic drugs (Buscopan) to decrease contraction of ureter and therefore decrease pain, treat cause, surgery (lithotripsy using high frequency sound waves).

109
Q

What is urinary incontinence?

A

Involuntary voiding

110
Q

What are 3 etiologic factors for urinary incontinence?

A

Stress incontinence, overflow incontinence, overactive bladder.

111
Q

What are the characteristics of stress incontinence?

A

Weak sphincter, increased intraabdominal pressure (violent coughing), change in uretho-vesicular angle (pelvic distend in pregnant women).

112
Q

What are the characteristics of overflow incontinence?

A

Intravesicular pressure > urethral pressure. Rentention + bladder distention.

113
Q

What are the characteristics of overactive bladder causing urinary incontinence?

A

Hyperactive detrusor muscle (can be a neural/myogenic problem)

114
Q

What are 2 treatment methods for urinary incontinence?

A

Drugs (fortify sphincter using alpha adrenergic agonist), surgery (artificial sphincter/prosthesis)

115
Q

What are two consequences of acute RF (ARF)?

A
  1. Fluid + electrolyte imbalance. 2. azotemia.
116
Q

Is ARF usually reversible? What is it defined as?

A

Yes. Loss of renal function.

117
Q

In ARF, what is oliguria defined as (in amount of urine prod per day) and anuria?

A

Olguria: 100-400 mL/day. Anuria:

118
Q

How many mLs of urine does one need to void per day to avoid azotemia?

A

400 mL/day

119
Q

What are 4 etiologic factors for PRERENAL ARF?

A

Hypovolemia, reduced vascular filling (septic/anaphylactic shock), HF, cardiogenic shock. Basically anything that results in reduced renal perfusion.

120
Q

What are 2 etiologic factors for INTRARENAL ARF?

A

Pyelonephritis, GN.

121
Q

What are 2 POSTRENAL ARF?

A

Ureteral obstruction, BPH.

122
Q

What percentage must the blood flow to the kidneys drop below in order to cause RF?

A

20%

123
Q

What is the patho for PRERENAL ARF?

A

Reduced renal perfusion leads to oliguria + ischemia

124
Q

What is the patho for INTRARENAL ARF? What are the 3 phases?

A

Initiating phase: from precipitation of event to when the manifestations present
Maintenance phase: reduced GFR, oliguria, problem is maintained.
Recovery phase: opposite of maintenance phase but very gradual, tissue repair results in gradual increase inGFR

125
Q

What is the patho for POSTRENAL ARF?

A

Obstruction to urine flow

126
Q

What are 7 manifestations of ARF?

A

Oliguria or anuria (may not always present this way), fluid + lyte imbalance, azotemia, edema, proteinuria, HTN, hematuria.

127
Q

What are the 4 treatment methods for ARF?

A

STAT treatment, replace fluid + lytes (monitoring very closely as kidneys are not fx properly), dialysis (peritoneal or hemo), diet modification (increase calorie, low protein + electrolytes).

128
Q

What is CRF? What stages does it progress through?

A

Irreversible + progressive damage to the kidneys. Diminished renal reserve, renal insufficiency, RF.

129
Q

What are the characteristics of the diminished renal reserve phase of CRF?

A

Renal fx is still adequate but it not fully fxing. GFR is less than 50% of normal. No signs of decreased renal fx.

130
Q

What are the characteristics of the renal insufficiency phase of CRF?

A

GFR between 20%-50% of normal

131
Q

What are the characteristics of the final phase of CRF (RF)?

A

GFR is less than 20% of normal. End stage of RF is when GFR is less than 5%

132
Q

How can STDs be transmitted?

A

Genitalia, mouth, rectum, skin, eye + placenta.

133
Q

What are high risk factors for STDs (6)?

A

Multiple sex partners, unsafe/high risk sexual partners, drug abuse, medically underserved, prior STDs, non-compliant STD treatment.

134
Q

What are low risk/no risks for STDs?

A

Abstinence, monogamy.

135
Q

What is genital herpes? What virus causes it? What cell does the microbe prefer to reside + multiply in? What must be in place in order to spread this STD? What is the incubation period of the virus? When do manifestations present after contact with the virus?

A

Recurrent systemic viral infection. Herpes simplex virus type II. Neurons. “Shedding lesion”. 2-10 days. 3-7 days.

136
Q

What are 4 manifestations of genital herpes?

A

Burning at site, painful vesicles, fever + muscle aches.

137
Q

What is an issue with the diagnosis of genital herpes? Is there a cure? What is a major problem when someone has this disease? What is the treatment for someone with genital herpes (2)?

A

It is sometimes subclinical (no manifestations). NO. Recurrence. Symptomatic treatment, and antivirals when flare up occurs to prevent further proliferation of the virus.

138
Q

What causes genital warts? Where are the warts located? What is the incubation period of the virus? Is there a cure? Are the lesions recurrent? Describe the lesions.

A

HPV virus strains 6 + 11. In the genital + anorectal region. 1-2 months. No. Yes. Benign, multiple growths resembling cauliflower.

139
Q

What is the treatment for genital warts (2)?

A

Remove warts (topical drugs - antimitotic + cytotoxic, surgery, cryotherapy) and monitor for cervical CA (strains 16 + 18 - it is likely the person will have contracted these strains)

140
Q

What is the MO that causes syphilis? What are the methods of spread? Can this be passed on to a fetus? If so, by which age gestation? What is the incubation period? Does this bacterium have a long or short generation time?

A

Treponema pallidum. Contact with lesions and across the placenta. Yes. Week 16 gestation. 60 - 90 days. Long generation time.

141
Q

What is a “generation time”?

A

Time it takes for bacterium population to double in size.

142
Q

What is unique about the microbe division + distribution?

A

It is systemic and will spread throughout the body via blood or lymph.

143
Q

What are complications of syphilis (4)?

A

Blindness, paralysis, heart disease + death.

144
Q

What are the 3 stages that syphilis goes through?

A

Primary, secondary, and tertiary stages.

145
Q

What are the characteristics of the primary stage of syphilis? Can the bacterium be eradicated at this stage?

A

Is the initial contact with the bacterium. Painless chancre at exposure site that heals in 3-12 weeks. Regional lymphadenopathy. Can eradicate bacterium at this stage.

146
Q

What are the characteristics of the secondary stage of syphilis? Can the bacterium be eradicated in this phase? What 6 manifestations? Can syphilis be diagnosed just based on some of the mnfts? What occurs during this phase that can last up to 50 years? What sets in?

A

6-8 weeks post infection, can last up to 6 months. MNFTS: maculopapular rash on palms + soles of feet, patches on mucous membranes, flat papules, generalized lymphadenopathy, fever + malaise. Yes. Latent period, damage progressively sets in.

147
Q

In the secondary stage of syphilis can the infected person still transmit the microbe?

A

Yes for the first 1-2 years from first contact, then after no.

148
Q

What are the characteristics of the tertiary phase of syphilis?

A

It is 1-35 years after untreated primary infection. Irreversible damage to bones, joints, CVS + neuro.

149
Q

How is syphilis treated?

A

Long acting penicillin (generation time).

150
Q

What is the MO responsible for chlamydia? What is the incubation? Why is detection difficult (2)? What is unique about this MO?

A

Chlamydia trachomatis. 7-21 days. 1. it is asymptomatic in most cases + 2. it is rudimentary = small + simple, difficult to isolate and detect. It is an obligatory intracellular bacterium, attempts to mimic a virus.

151
Q

What are 3 chlamydial manifestations for males? 4 for females? Which is a complication?

A

MALES: white or clear discharge, mild dysuria, testicular pain. FEMALES: mucopurulent vaginal discharge, dysuria, bleeding, pelvic pain (PID - complication).

152
Q

How is chlamydia treated?

A

Doxycycline or azithromycin.

153
Q

What is the MO causing gonorrhea? What is the incubation time? This has a large carrier population, what does that mean? Are the infection symptoms local or systemic?

A

Neisseria gonorrhoeae. 3-8 days. No manifestations but pass on MO. Both local and systemic mnfts.

154
Q

What are 4 female manifestations of gonorrhea? Which is a complication for females? 2 for males?

A

FEMALES: Purulent vaginal discharge, dysuria, genital irritation, late pelvic pain (PID - complication). MALES: urethral discharge, dysuria.

155
Q

What are 3 systemic manifestations of gonorrhea? Which is a complication?

A

Bacteremia, pharyngeal or conjunctivitis (oral sex or contaminated hands), arthritis-dermatitis syndrome (complication).

156
Q

What is arthritis-dermatitis syndrome?

A

Septic arthritis. Bacteria enters join + causes infection. Accompanied by inflammation of the skin (dermatitis).

157
Q

What is the first line treatment for gonorrhea? What is the second line treatment?

A

Cephalosporins (becoming resistant). Increase dose of cephalosporins + add another class of abx.

158
Q

What virus causes AIDS? Which part of the immune system is targeted? Where are the major reservoirs for this virus? Is there a cure? What does “retrovirus” refer to?

A

Human immunodeficiency virus (HIV). T helper cells. Semen and blood. No cure. It transcribes DNA backwards, from RNA to DNA, rather than from DNA to RNA, the virus has RNA in it.

159
Q

What two strains of the retrovirus are there? What 4 ways can this virus be acquired? How can HIV be acquired through labour + delivery? In the occupational domain, what 3 things depend on whether or not the virus is acquired in a needlestick injury?

A

HIV 1 + HIV 2. Sexual, contaminated blood, maternal (in utero, labour + delivery, lactation). “Shedding lesions” in labour and delivery if placenta detaches and contaminated blood comes in contact with fetus will pass on to fetus. 1. site (absorption) 2. depth of injury 3. viral load (# of viral particles on needle).

160
Q

What are the three phases of the patho for AIDS?

A

Primary infection, latent period, and over AIDS.

161
Q

What are the characteristics/patho for primary infection of AIDS? How long can this stage last?

A

Its the initial contact with the virus. This stage can last wk-months. Window period (time for enough Abs to be made to be detected diagnostically) and seroconversion (process of Ab formation) occur during this phase. The viral load is high + CD4 count is low

162
Q

What is CD4 count in AIDS?

A

CD4 are the surface receptors on the T helper cells, able to measure the protein count (CD4) which will tell you how many T helper cells you have.

163
Q

Is the viral load inversely proportional, or proportional to CD4 count?

A

Inversely proportional.

164
Q

What are the characteristics/patho of the latent period in AIDS? What are 2 manifestations that occur during this phase?

A

The person is asymptomatic for years. There is damage to lymphatic tissue, recurrent respiratory infections as microbes are constantly in contact with the RT. Fatigue.

165
Q

When will the overt AIDS period commence approximately? What is targeted during this phase? What is the patho for overt AIDS? Is this multi-organ damage?

A

Around 10 years. T helper cells, macrophages, and B cells are targeted. Immune system is destroyed resulting in a decreased immunity and defences resulting in lots of new infections (opportunistic) and infections from latent pathogens. Yes.

166
Q

What is the issue that occurs in AIDS when macrophages are affected? B cells?

A

MACROPHAGES: compromised early non-specific defences. B CELLS: issue with Ab production.

167
Q

What 5 things can be used to diagnose AIDS?

A

Clinical presentation, Western blot assay, ELISA, PCR, CD4 counts & viral load.

168
Q

What is the ELISA? What does it stand for? What does it test for?

A

Enzyme Linked Immunosorbent Assay. It tests for Abs against the virus + measures the amount of them. Measures ALL Ab against ALL antigens on the virus = not extremely specific.

169
Q

What is the Western blot assay?

A

Measures one specific Ab that has been produced for one specific Ag on the HIV virus.

170
Q

What does PCR stand for? What does it do?

A

Polymerase chain reaction. It measures the genetic composition of the HIV virus.

171
Q

What are the WHOs standards for AIDS?

A

Patient must have over 20 infections in place in order to be considered to have AIDS - some may be latent, do not all have to be at same time.

172
Q

What are the CDCs standards for AIDS?

A

The T helper cell count must drop below a specific threshold and the individual must have one or two opportunistic CA or infections in place.

173
Q

What is a manifestation of AIDS? 2 manifestations of the RT? 2 GI? 2 NS? Which opportunistic CA may be in place in someone with AIDS?

A

Opportunistic infections. TB + pneumonia. Gastroenteritis + diarrhea. Dementia + encephalopathy. CANCERS: Kaposi’s Sarcoma, NHL, cervical CA.

174
Q

In Kaposi’s Sarcoma, where does the malignancy arise? Where else can these lesions be found?

A

Endothelium of BVs. Not limited to BV, also appear on skin, lymph nodes + mucous membranes in the mouth.

175
Q

Why is opportunistic CA a thing in AIDS?

A

Because since the immune system is suppressed, malignant cells cannot be destructed.

176
Q

What is the treatment for AIDS?

A

Cocktail of antivirals to target different phases in cell proliferation. “Retro-antivirals” Limit progression of the disease.

177
Q

What is primary amenorrhea described as?

A

Failure to menstruate by age 15, or failure to menstruate by age 13 with no secondary sex characteristics.

178
Q

What are 4 etiologic factors for primary amenorrhea?

A

Gonadal dysgenesis, congenital mullerian agenesis, testicular feminization + hypothalamic-pituitary-ovarian axis disorder.

179
Q

What is secondary amenorrhea described as?

A

Cessation of menses for at least 6 months in a woman that has established normal menstrual cycles.

180
Q

What are 6 etiologic factors for secondary amenorrhea?

A

Ovarian, pituitary, or hypothalamic dysfx; intrauterine adhesions, infections (TB/syphilis), pituitary tumor, anorexia nervosa, extrenuous activity.

181
Q

How is amenorrhea usually treated?

A

BCP.

182
Q

What is dysmenorrhea?

A

Painful menstruation

183
Q

What is primary dysmenorrhea?

A

Menstrual pain that is not associated with a physical abnormality or pathological process.

184
Q

Why are prostaglandin synthetase inhibitors important for primary dysmenorrhea?

A

Prostaglandin causes painful uterine contraction + arteriolar vasospasm.

185
Q

What is secondary dysmenorrhea? 6 etiologic factors?

A

Menstrual pain caused by specific organ diseases. Endometriosis, uterine fibroids, adenomyosis, pelvic adhesions, IUDs, PID.

186
Q

What is the treatment for secondary dysmenorrhea?

A

Identify + correct underlying problem.

187
Q

What is menorrhagia? What is an etiologic factor for young women? Older women?

A

Prolonged or excessive bleeding during the normal menstrual cycle. YOUNGER: Endocrine disturbances. OLDER: inflammatory disorder, tumor of uterus, hormonal imbalance.

188
Q

What is metorrhagia? What are etiologic factors for it?

A

Vaginal bleeding outside of the normal menstrual cycle. May signal CA, or benign tumors of the uterus.

189
Q

What are 4 risk factors for bladder cancer? Is the true etiology known?

A

Smoking, chronic UTI + bladder stones, carcinogens excreted in urine stored in bladder, Schistosoma haematobium. No idiopathic.

190
Q

What are the two categories of bladder cancer?

A

Low-grade non-invasive + high-grade invasive tumors.

191
Q

What are the characteristic of high-grade bladder cancer tumors? Cells of origin? Where does this cancer invade? Will it mets? How many individuals with this type of cancer progress to an invasive disease?

A

Transitional (urothelium) cells lining bladder. Will invade into bladder wall + mets. 15-40% of people will develop invasive disease.

192
Q

What are the characteristics of low-grade non-invasive bladder cancer tumors? Cell of origin? Will it recur after resection? Prognosis?

A

Transitional (urothelium) lining of bladder. It may recur. Good prognosis, less than 5% progress to high-grade tumors.

193
Q

What is the most common manifestation of bladder cancer? 3 others?

A

Painless hematuria. Frequency, urgency, dysuria.

194
Q

What is a screen for those at risk for bladder cancer? 7 other diagnostics?

A

Periodic urine cytology. Cytology, excretory urography, biopsy, cystoscopy, US, CT + MRI.

195
Q

What are 4 treatment methods for bladder cancer?

A

Diathermy (electrocaudery), surgical resection, chemo instilled in bladder, cystectomy + resection of pelvic lymph nodes.

196
Q

What type of tumor is the Wilms tumor? Who is this most common in? Does this tumor occur in one or both kidneys? What is the tumor comprised of? What congenital anomalies is this tumor associated with?

A

Nephroblastoma. Children 3-5. Can occur in one or both kidneys. Combination of blastemic, stromal, and epithelial tissue. Associated with aniridia, and hemihypertrophy.

197
Q

What is the appearance + growth of the Wilms tumor like?

A

Solitary mass appearing in any part of kidney, sharply demarcated + variably encapsulated. Will grow to a large size.

198
Q

What are the manifestations of Wilms tumor?

A

HTN, large asymptomatic abdominal mass.

199
Q

What is the treatment for Wilms tumor?

A

Surgery, chemo + radiation sometimes.

200
Q

Renal cell carcinoma accounts for what percentage of all kidney tumors? What part of the kidney is commonly affected? During early stages is this a quietly advancing cancer or no? What do manifestations usually denote?

A

90-95%. The upper pole. Yes. Denote advanced disease.

201
Q

What 5 types of renal cell carcinomas are there? Which is the most prevalent?

A

Clear cell carcinoma, papillary tumors, chromophobic tumors, oncocytomas, collecting duct tumors. Clear cell carcinoma (60%).

202
Q

What are the characteristics of clear cell carcinoma? Cell of origin? What sort of genetic mutation occurs? What is unique about the malignant cells?

A

Proximal tubular epithelial cells. Chromosome 3 deletion. Tumor cells have a clear cytoplasm.

203
Q

What is the most common manifestation of renal cell carcinomas? What are 2 other manifestations?

A

Hematuria. Flank pain + presence of palpable flank mass.

204
Q

How is renal cell carcinoma diagnosed?

A

US, CT

205
Q

What are 2 treatment methods for renal cell carcinoma?

A

Surgery (radical nephrectomy + lymph node dissections), and immunotherapy.

206
Q

What is the bacteria called that causes syphilis? What type of bacteria is this? How does it affect treatment?

A

Treponema pallidum. Spirochetes. Long generation time = long acting penicillin.

207
Q

What is the bacteria called that causes chlamydia? What type of bact. is this? What is special about this bacteria (2)?

A

Chlamydia trachomatis. Gram negative. Intracellular bacteria, mimic virus, rudimentary = difficult to isolate.

208
Q

What bacteria causes gonorrhea? What type of bacteria is this?

A

Neisseria gonorrhoeae. Gram negative diplococcus.

253 (6 decks)

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