Pathology

Question 1

What are 4 pathological states leading to urinary tension?

What is a pathological state leading to urinary incontinene?

Answer 1

Tension

1. Anticholinergic medications (ex. atropine, gravol, ipatropium)
2. Spinal cord injury
3. Diabetics
4. Stroke damaging the pontine micturition center

Incontinence

1. Stroke damaging the pontine storage center

Question 2

Define the following:

Urinary Tract Infection

Urethritis

Cystitis

Acending pyelonephritis

Pyelonephritis

Asymptomatic Bacteriuria

Answer 2

UTI = an infection affecting part of the urinary tract

Cystisis = an infection of the bladder

Ascending pyelonephritis = UTI affecting the ureters on the way up to the kidneys

Pyelonephritis = an infection of the kidneys

Asymptomatic Bacteriuria = presence of bacteria in urinary tract in the absence of symptoms

Question 3

What makes a UTI “complicated” (4)

Answer 3

1. Presence of DM
2. Pregnancy
3. Male
4. Immunocompromised

Question 4

Epidemiology of UTI

1. How many million people have a UTI each year globally?
2. What % of women have a UTI in a given year?
3. What % of women have a UTI over their lifetime
4. Sexual activity causes what % of bladder infections in young sexually active women?
5. What is the age range with the most frequent UTIs?

Answer 4

1. 150 million
2. 10%
3. 50%
4. 75-90%
5. 16-35

Question 5

Why do women have an increased risk of a UTI than men? Why does this risk increase with age?

Answer 5

The shorter urethra makes it more likely for a pathogen to invade.

Post-menopausal loss of estrogen leads to the loss of protective vaginal flora

Question 6

1. What bacteria is the most common cuase of a community-acquired UTI? Second most common?
2. What 2 bacteria are more likely to be the culprit of a blood-borne UTI?
3. What are 2 types of bacteria that can cause urethritis but not cystitis?

Answer 6

1. E. Coli, Staphylococcus Saprophyticus
2. Staphylococcus Aureus, Salmonella
3. Chlamydia trachomatis, Mycoplasma genitalium

Question 7

What are the gram negative bacteria that can cause a UTI? Gram positive?

Question 8

What factors increase your risk of developing a UTI? (11)

Answer 8

1. Urinary catheter (Foley)
2. Sexual intercourse
3. Divers using condom catheters or external catching devices
4. Female gender
5. Diabetes (inhibition of neutrophils)
6. Obesity
7. Family history
8. Lack of circumcision
9. Impaired bladder emptying
10. Distortion of veiscoureteral junction either from a past infection or a congenital malformation
11. Chronic prostatitis

Question 9

What 5 organisms are associated with a UTI in the context of a catheter?

Answer 9

1. E. Coli
2. Klebsiella
3. Pseudomonas
4. Candida albicans
5. Enterococcus

Question 10

What is a vesicoureteral reflux?

Answer 10

The backflow of urine from the bladder and up the ureters

Question 11

What is the pathogenesis of a UTI?

Answer 11

1. Bacteria enter the urethra (usually from the bowel) and travels to the bladder or gains access to the tract via blood or lymph
2. Once in the bladder, they create a biofilm by attaching their pili to toll-like receptors. This increases their reistance to our immune system
3. Neutrophils attempt to clear the pathogen

Question 12

What are symptoms of a lower UTI?

Answer 12

1. Burning (pain) with urination
2. Increased frequeny and urgency of urination
3. Difficulty urinating
4. Feeling the need to urinate in the absene of a full bladder
5. Suprapubic and lower back pain
   (6. Blood/pus in urine –> rare)

Question 13

What are the symptoms of a kidney infection?

Answer 13

1. Fever with a high spiking pattern and termination after 3 days of treatment
2. Nausea and vomiting
3. Flank pain and pain at the costovertebral angle
4. Lower UTI symptoms
   (5. Blood/pus in the urine –> rare)

Question 14

What are indications of a UTI in children? Elderly?

Answer 14

Children = fever, poor feeding, vomiting, poor sleeping, fussy, jaundice, new onset urinary incontinence or regression in potty training

Eldelry = delirium, fatigue, fever, chills, and incontinence

Question 15

What are 6 possible investigations for a UTI?

Answer 15

1. Urinalysis = leukocyte esterase and nitrites, (white blood cell casts indicate pyelo)
2. Urinalysis with microscopy = >2(m)-10(f) wbc/HPF, rbc
3. Urine culture = 100,000 CFU/mL
4. Renal U/S = hydro-nephrosis, malformations
5. Voiding cystourethrogram = injection of dye with real-time X-ray during urination
6. Renal scintigraphy with DMSA = kidney scarring

Question 16

When is it indicated to do a urinary culture when you are suspicious of a UTI? (5)

Answer 16

1. Pregnant females
2. All females under 2 years of age
3. Uncircumcised males under 1 year of age (but really all males)
4. Those presenting with recurrent UTIs
5. Elderly with signs of systemic infection and advanced dementia preventing communication

Question 17

What are complications that can arise from a UTI? (7)

Answer 17

1. If during pregnancy, pyelonephritis is more likely to occur
2. If during pregnancy, risk of low birth weight or premature infant
3. Permanent kidney damage
4. Renal papillary necrosis if a kidney infection
5. Urethral narrowing in men
6. Bacteremia
7. Sepsis

Question 18

What are 5 things you can give to someone with a UTI?

What are 3 types of preventative measures for a UTI?

Answer 18

Treatment:

1. Antibiotics
2. Methenamine
3. Phenazopyridine
4. Acetaminophen
5. Topical vaginal estrogen

Prevention:

1. Drinking lots of fluids
2. Good hygiene (wiping from urethra to rectum in women)
3. Urinate right after sexual intercourse

Question 19

How do you treat asymptomatic bacteriuria?

Answer 19

Only treat if pregnant or after a urological procedure.

1. Get urine culture
2. Treat with amoxicillin or nitrofurantoin

Question 20

How do you treat cystitis?

Answer 20

Uncomplicated = short course of antibiotics

Complicated = long term of IV antibiotics

Question 21

How do you treat pyelonephritis?

Answer 21

Antibiotics

Question 22

How do you treat a perinephric abscess?

Answer 22

1. IV antibiotics
2. Incision and drainage of the abscess

Question 23

What are some examples of gram-negative bacteria? What are some examples of gram-positive bacteria? How can you tell which bacteria type has caused a UTI?

Answer 23

Gram negative:

= E. Coli, Klebsiella, proteus, enterobacter, citrobacter, salmonella

Gram positive:

= Enterococcus, staphylococcus saprophyticus, staphylococcus aureus

Gram negative bacteria produce nitrites

Question 24

What is Pasternacki’s sign?

Answer 24

Pain at the costovertebral angle

Question 25

What is prostatitis?

What is chronic pelvic pain syndrome?

Answer 25

Acute or chronic infectious and non-infectious abnormalities of the prostate gland leading to enlargement.

When non-infectious, they are referred to as chronic pelvic pain syndrome.

Question 26

What causes infectious prostatitis? (broadly speaking)

Answer 26

Bacteria

Question 27

What is the presentation of prostatitis? (acute vs. chronic)

Answer 27

Acute:

• Dysuria
• Increased frequency/urgency of urinating
• Pain in the prostatic pelvic or perineal area
• Fever and chills
• Symptoms of bladder outlet obstruction

Chronic:

• Recurrent episodes of cystitis
• Pain in the prostatic pelvic or perineal area

Other:

• Cloudly/bloody urine
• Abdominal pain
• Pain in penis or testicles
• Painful ejaculation

Question 28

What is the nephrotic syndrome?

What is the difference between primary and secondary nephrotic syndrome?

What is the nephrotic tetrad seen in this syndrome?

Answer 28

Syndrome = proteinuria, hypoalbuminemia, peripheral edema

Primary = idiopathic, secondary = caused by something we know

Tetrad = the above 3 + hypercholesterolemia

Question 29

Are adults or children more affected by nephrotic syndrome? Men or women?

What is the most common disease causing nephrotic syndrome in children? adults?

Answer 29

Adults, men

Children = 70-90% from minimal change disease

Adults = 30-40% from membranous glomerulonephritis

Question 30

What is glomerulonephritis?

Answer 30

Acute inflammation of the kidney, typically due to an immune response

Question 32

What is minimal change disease? Describe the pathogenesis.

Answer 32

A type of nephrotic syndrome characterized by podocyte effacement and caused by a T-cell mediated process

The loss of negative podocytes allows albumin to move into the Bowman’s capsule

Question 33

What is membranous glomerulonephritis? Describe the pathogenesis.
What are some secondary causes of it?

Answer 33

A type of nephrotic syndrome characterized by inflammation and spike-like thickening of the glomerular basement membrane.

Subepithalial deposits (antigen-antibody complexes) activate the complement system which creates a membrane attack complex. This complex damages podocytes and mesangial cells and recruits other inflammatory cells. All together, the GBM is damaged and leaky to proteins.

Secondary = infection, malignancy, autoimmune condition, medications

Question 34

What is focal segmental glomerulosclerosis? Describe the pathogenesis.

What are some secondary causes of it?

Answer 34

A type of nephrotic syndrome characterized by sclerosis affecting only parts of only some glomeruli.

Podocyte damage (idiopathic) allows proteins and lipids to pass by. Some get trapped in the space around the capillaries causing hyalinosis. Over time the trapped molecules develop into sclerosis.

Secondary = sickle cell disease, HIV-nephropathy, heroin-nephropathy, kidney hyperperfusion, increased glomerular capillary pressure

Question 35

What are 6 outcomes of mass proteinuria and how do they occur?

Answer 35

1. Low albumin = loss into urine
2. Hypercholesterolemia = liver over-active to replace albumin
3. Edema = decreased plasma oncotic pressure from low albumin so that water moves into interstitium

Edema –> decreased CO –> decreased renal blood flow –> decreased GFR –> RAAS –> increased water re-absorption –> worsening edema

4. Hypovolemia = decreased plasma oncotic pressure from low albumin so that fluid moves into interstitium
5. Increased risk of infection = loss of antibodies into urine
6. Hypercoagulable state = greater loss of antithrombin than clotting factors

Question 36

How does nephrotic syndrome present? (11)

Answer 36

Proteinuria

1. Frothy urine

Hypercholesterolemia

2. Xanthelasma
3. Xanthomata

Hypoalbuminemia

4. Tiredness
5. Cachexia
6. Leukonychia

Peripheral edema

7. Periorbital swelling
8. Ascites
9. Pitting
10. Breathlessness (pulmonary edema, pleural effusion)
11. Arthralgia

Question 37

What are diagnostic findings in nephrotic syndrome for:

1. Urinalysis
2. Blood analysis
3. Chest X-ray
4. Renal U/S

Answer 37

1. elevated (>3.5 g/day) protein, urine Ig, urinary casts
2. Low (<2.5g/dL) albumin, high urine protein/creatinine, high cholesterol (LDL/VLDL), LFT showing heightened liver function, possibly low Ca++, possibly high CRP, possibly high glucose (fasting/HbA1)
3. Possibly pleural effusion and/or pulmonary edema
4. Possibly damage/congenital abnormality?

Question 38

Fill out the following chart for nephrotic syndrome renal biopsy:

Answer 38

Question 39

What are possible complications of nephrotic syndrome? (10)

Answer 39

1. Thromboembolic disorder from decreased antithrombin
2. Infection from lost immunoglobulins (peritonitis > lung > skin > UTI > miningoencephalitis > sepsis)
3. Acute kidney failure from hypovolemia
4. Pulmonary edema
5. Hypothyroidism from lost thyroxine
6. Vitamin D deficiency and resulting hypocalcemia
7. Microcytic hypochromic anemia from lost iron
8. Protein malnutrition and wasting
9. Growth retardation from lost hormones
10. Cushing’s syndrome from the body trying to compensate with the RAAS

Question 40

Nephrotic syndrome treatment:

1. What is the first line treatment for minimal change disease in children?
2. What is another option for treatment (especially frequent relapsers)
3. Should steroids be used to treat membranous glomerulonephritis? Focal segmental glomerulosclerosis?

Answer 40

1. Steroids (8 week course)
2. Alkylating agent (ex. cyclophosphamide)
3. Yes but treat underlying disease; Unsure –> inconsistent results

Question 41

How do you treat the different components/complications in nephrotic syndrome?

Answer 41

Question 42

What is pre-renal acute kidney injury refer to?

Answer 42

Kidney injury due to decreased blood flow into the kidneys

Question 43

What are causes of pre-renal acute kidney injury?

Answer 43

1. Absolute fluid loss (hemorrhage, vomiting, diarrhea, burns, low intake)
2. Relative loss of fluid (distributive shock, CHF)
3. Renal artery problems (stenosis, embolus)
4. Medications (ACEi, NSAIDs)
5. Hypotension

Question 44

What happens in pre-renal AKI?-

Answer 44

Less blood gets to the kidnesy and the GFR drops. This causes:

• High levels of nitrogen in the blood (azotemia)
• Low urine excretion (oliguria)
• RAAS activation and resultant increase in BP
• Urea reabsorption

Question 45

Fill in the following lab findings for pre-renal AKI:

Answer 45

Question 46

How do you treat pre-renal AKI?

Answer 46

1. Determine if they are volume high or low
2. If high give diuretics; if low give IVF
3. Correct the underlying cause

Question 47

What are 4 main reasons for administering diuretics?

What are 8 other reasons?

Answer 47

1. Decrease expanded EC volume (edema)
2. Decrease blood pressure
3. Increase urinary excretion of excess ions
4. Prevent anuria in acute renal failure

Dialysis disequilibrium syndrome, calcium nephrolithiasis, osteoporosis, nephrogenic diabetes insipidus, epilepsy, metabolic alkalosis, altitude sickness, cystic fibrosis

Question 48

What is hypertension a risk for? (5)

Answer 48

1. CAD
2. Stroke
3. Heart failure
4. Renal disease
5. Peripheral vascular disease

Question 49

What is the difference between essential and secondary hypertension?

How do you differentiate between them?

Answer 49

Essential = cause of the BP elevation is unknown (90% of cases)

Secondary = known problem is causing elevated BP

Question 50

What are the indications for:

1. Pre-hypertension
2. Hypertension stage I
3. Hypertension stage II
4. Hypertensive urgency
5. Hypertensive emergency

Answer 50

1. SBP > 120; DBP > 80
2. SBP > 135; DBP > 85
3. SBP > 140; DBP > 90
4. BP > 180-220/120 with no signs of end organ damage
5. BP > 180-220/120 with signs of end organ damage

Question 51

What are 5 non-modifiable and 9 modifiable risk factors for high blood pressure?

Answer 51

Non-modifiable:

1. Family history positive
2. Older age
3. Male gender
4. African American race
5. Chronic kidney disease

Modifiable:

1. Lack of physical activity
2. Unhealthy diet (high in sodium)
3. Overweight/obese (strain on CV system)
4. Excess alcohol intake
5. Sleep apnea
6. High cholesterol
7. Diabetes
8. Smoking/tobacco
9. Stress

Question 52

What things are considered to be “end-organ damage”? (6)

Answer 52

1. CHF
2. LVH
3. Aortic dissection
4. Kidney failure
5. Pulmonary edema
6. Retinal hemorrhage

Question 53

What are 3 possible causes of primary hypertension?

Answer 53

1. Genetics (complex polygenic disorder, RAAS genes)
2. Defects in regulation (SNS+, abnormal vascular tone regulators, abnormal ion channels, inappropriate hormone regulation, problems with sensors, abnormal CNS control)
3. Insulin resistance and obesity (angiotensinogen released from adipocytes, increased viscosity, insulin activating SNS)

Question 54

What is part of your work-up in investigating possible causes of secondary hypertension?

Answer 54

1. General screening
2. Urinalysis and serum creatinine
3. Electrolytes (low K+)
4. Blood analysis (BUN, glucose, cholesterol, triglycerides)
5. Hormone levels (24 hour urine cortisol, TH, PTH, 24 hour urine metanephrines, GH)
6. Sleep study
7. Bood pressure differences from R to L arm and arm to leg

Question 55

What are 4 big categories for possible causes of secondary hypertension?

Answer 55

1. Exogenous (medications)
2. Renal cause (damage, RAAS)
3. Mechanical cause
4. Endocrine cause

Question 56

What are 8 possible exogenous causes of secondary hypertension and how do they increase BP?

Answer 56

1. Oral contraceptives = estrogen increases angiotensinogen synthesis
2. Glucocorticoids = increased SNS
3. Cyclosporine
4. Erythropoietin = increased blood viscosity
5. Sympathomimetic drugs = increased SNS
6. NSAIDs = augmentation of renal sodium/water retention
7. Ethanol = increased SNS
8. Cocaine = increased SNS
9. Tyrosine kinase inhibitors

Question 57

What are 2 major renal causes of secondary hypertension? How do they lead to high blood pressure?

How would you investigate?

Answer 57

1. Renal parenchymal disease = damaged nephrons can’t excrete sodium and water –> increased BV –> increased BP

Investigations = low Na+ in urine and high Na+ in serum; possible proteinuria

2. Renal arterial stenosis = blocking renal flow and causing RAAS activation

Investigations = abdominal bruit, hypokalemia, elevated aldosterone, imaging

Question 58

What are 2 mechanical causes of secondary hypertension? How do they lead to high blood pressure?

How would you investigate?

Answer 58

1. Coarctation of the aorta = decreased renal flow –> RAAS activation (possibly blunted baroreceptor response to increased BP)

Investigations = BP differences, claudication, fatigue, weak/absent femoral pulse, mid-systolic murmur, imaging

2. Obstructive sleep apnea –> fatigue and glucocorticoid release or hypoventilation and hypercapnia

Investigations = sleep study

Question 59

What are 7 endocrine causes of secondary hypertension?

Answer 59

1. Pheochromocytoma
2. Primary aldosteronism (ex. Conn Syndrome, bilateral hyperplasia)
3. Secondary aldosteronism (ex. renin-secreting tumor, chronic liver disease)
4. Glucocorticoid-remediable aldosteronism
5. Cushing syndrome
6. Thyroid abnormalities
7. Acromegaly

Question 60

Explain how the following endocrine causes lead to secondary hypertension. How would you investigate? How would you treat?

Answer 60

Question 61

What are possible symptoms of progressive hypertension? (6)

Answer 61

1. Sweating
2. Headache
3. Dizziness
4. Epistaxis
5. Flushing
6. Blurred vision

*Usually asymptomatic until an event or routine exam

Question 62

What are the complications of hypertension?

Answer 62

Question 63

What is the pathogenesis of kidney injury as a result of hypertension?

Answer 63

1. Vessel walls become thickened with hyaline infiltrate
2. Increased hypertension induces smooth muscle hypertrophy and necrosis of capillary walls (fibrinoid necrosis)
3. This reduces the vascular supply to the kidney
4. Ischemic atrophy of the tubules and glomeruli then occur

Question 64

What is hypertensive encephalopathy?

Answer 64

Increased intracranial pressure from elevated BP resulting in headache, blurred vision, confusion, somnolence, and coma

Question 65

What is accelerated-malignant hypertension?

Answer 65

Hypertension resulting in acute damage to retinal vessels and presenting with hemorrhage, exudate, and sometimes papilledema on fundoscopy

Question 66

What are some non-pharmacologic treatments for hypertension?

Answer 66

1. Weight reduction
2. Exercise
3. Diet (High K+, Ca++, Mg++; low caffeine, salt, alcohol)
4. Smoking cessation
5. Relaxation therapy

Question 67

What are 4 classes of drugs used in treating hypertension?

Answer 67

1. Diuretics
2. Sympatholytics
3. Vasodilators
4. RAAS blockade

Question 68

How do diuretics improve hypertension?

What type of hypertensive patient would be given a diuretic?

Answer 68

Thiazides and potassium sparing diuretics promote Na+ excretion and thus water excretion

(Loop diuretics are too potent and short-lived)

Patient = mild to moderate hypertension; normal renal function; salt sensitive people

Question 69

How do sympatholytics improve hypertension?

What type of hypertensive patient would be given a sympatholytic?

Answer 69

Beta blockers reduce HR and contractility and thus CO which decreases renin

Central alpha-adrenergic agonists reduce SNS signaling to heart, vasculature, and kidney

Systemic alpha-adrenergic blockers relax vascular smooth muscle

Patient = older men shoulduse systemic alpha blockers

Question 70

How do vasodilators improve hypertension?

Answer 70

Calcium channel blockers reduce cardiac heart contraction and vascular smooth muscle contraction

Hydralizine and minoxidil directly relax vascular smooth muscle of precapillaries

Question 71

How do RAAS blockade drugs improve hypertension?

What type of hypertensive patient would be given a RAAS blockade?

Answer 71

ACE inhibitors block angiotensin II production which reduces systemic vasoconstriction and water retention

Angiotensin II receptor blockers reduces systemic vasoconstriction and water retention

Direct renin inhibitors reduce systemic vasoconstriction and water retention

Patient = slows down renal failure in diabetic nephropthy

Question 72

What is renal artery stenosis?

Answer 72

The narrowing of one or both of the renal arteries

Question 73

What are the 2 most common causes of renal artery stenosis?

Answer 73

1. Atherosclerotic renal artery disease (~90%)

Fat, calcium, and immune cells form a crusty rim around inside of artery, usually at beginning

2. Renal Fibromuscular Dysplasia (~10%)

Fibrous collagen, connective tissue, and smooth muscle develop abnormally causing a series of bluges, usually at middl to distal end

Question 74

What are some uncommon but possible causes of renal artery stenosis? (6)

Answer 74

1. Vasculitis
2. Neurofibromatosis
3. Congenital bands
4. Extrinsic compression
5. Radiation
6. Embolus

Question 75

What is the pathophysiology of renal artery stenosis?

Answer 75

1. Narrowing of renal afferent decreases renal blood flow
2. JG cells release renin –> RAAS
3. RAAS causes systemic and renal constriction
4. This maintains GFR at first, but continual constriction leads to systemic hypertension
5. Complications such as stroke and heart attack can then occur

Question 76

What are some complications of renal artery stenosis?

Answer 76

1. Renal ischemia –> renal atrophy –> fibrosis
2. Stroke from systemic hypertension
3. Heart attack from systemic hypertension

Question 77

What are the signs and symptoms of renal artery stenosis?

Answer 77

Usualy asymptomatic

May have a headache and blurry vision from hypertension

May have flash pulmonary edema brought on by a palliating factor

Question 78

How do you diagnose renal artery stenosis?

Answer 78

1. Renal bruits
2. Urinalysis (high serum creatinine, hypokalemia, protein hyaline, casts)
3. Imaging (atrophy, malformations)
4. Renal arteriography (visualize arteries for the blockage)
5. Captopril challenge test (high renin baseline, decreased renin clearance in response to captropril, an ACE inhibitor)

Question 79

What is the treatment for renal artery stenosis?

Answer 79

1. Medications aimed at managing hypertension (diuretics, ACEi, ARBs, vasopressors, sympatholytics)
   - Be careful using a RAAS blockade (25-30% rise in creatinine is ok)
2. Healthy eating and exercise
3. Surgery (balloon angioplasty +/- stent, bypass, removal)
4. Atherosclerotic medications (aspirin, statins)

Question 80

What is metabolic acidosis? What are two different types?

Answer 80

MA = a decrease in serum HCO3- causing pH to lower to <7.35

High anionic gap = decreased pH caused by excess H+ that isn’t part of the anion gap

Non-anionic gap = decreased pH due to loss of HCO3- (offset by increased Cl-)

Question 81

What are causes of high anionic gap metabolic acidosis? (13)

Answer 81

MUDPILES CT / GOLDMARK

• Glycols (ethylene, poly, propylene)
• 5-Oxoproline (chronic acetaminophen ingestion)
• Lactate
• D-lactate (short gut syndrome)
• Methanol
• Aspirin (salicylates)
• Renal failure
• Ketoacidosis
• Uremia (sulphates, phosphates)
• Paraldehyde
• Carbon monoxide
• Cyanide
• Toluene
• Massive rhabdomyolysis

Question 82

What are causes of non anionic gap metabolic acidosis? (10)

Answer 82

USED CRAP

• Ureterosigmoidostomy
• Small bowel issues
• Extra chloride administration
• Diarrhea
• Carbonic anhydrase inhibitors
• Renal tubular acidosis
• Addison’s disease (hyperkalemia)
• Pancreatic issues
• Parenteral nutrition
• Paraprotein states

Question 83

How do you determine whether a non-anionic gap metabolic acidosis has a renal etiology or non-renal etiology?

Answer 83

Renal = positive urine anionic gap

Non-renal = negative urine anionic gap

Question 85

How does the body compensate in metabolic acidosis and what is the result of these compensations? (3)

Answer 85

1. Increased absorption of H_ into renal cells –> hyperkalemia
2. Increased respiratory rate and depth –> increased minute ventilation, decreased CO2
3. Renal compensation –> decreased Na+ and water uptake

Question 86

What are signs/symptoms of metabolic acidosis? (7)

Answer 86

• Headache
• Altered mental status
• Decreased visual acuity
• Chest pain/palpitations
• Kussmaul respiration
• Nausea/vomiting, abdominal pain, altered appetite, weight gain
• Muscle weakness, bone pain, joint pain

Question 87

What are serious neurological complications of metabolic acidosis? Cardiac complications?

Answer 87

Neural = coma, seizures

Cardiac = ventricular tachyardia, hypotension

Question 88

How do you treat a metabolic acidosis?

Answer 88

1. IV bicarbonate (50-100 mmol at time –> be careful of ABG readings)
2. Dialysis if necessary (kidney failure or OD)
3. Treat the underlying cause

Question 89

What is metabolic alkalosis? What are two different types?

Answer 89

Metabolic alkalosis = an increase in serum HCO3- causing pH to increase to > 7.45

Chloride-responsive MA = chloride lost along with H+ (urine Cl- <10 mEq/L)

Chloride-resistant MA = chloride retained; retention of HCO3- primarily responsible (urine Cl- > 20 mEq/L)

Question 90

What are causes of chloride-responsive metabolic alkalosis? (6)

Answer 90

• Diarrhea
• Vomiting
• Contraction alklaosis
• Post-hypercapnia
• Cystic Fibrosis
• Excess ingestion of antacids

Question 91

What are causes of chloride-resistant metabolic alkalosis? (2)

Answer 91

• Hypokalemia
• Excess aldosterone (adrenal tumor, pheochromocytoma, congenital adrenal hyperplasia, Cushing’s)

Question 92

How does the body compensate in metabolic alkalosis and what is the result of these compensations? (3)

Answer 92

1. Increased secretion of H+ from cells –> hypokalemia
2. Decreased respiratory rate and depth –> decreased minute venitlation and increased CO2
3. Renal compensation –> retention of H+

Possible water gain; possible water loss

Question 93

What ion is used to assess volume status in metabolic alkalosis?

Answer 93

Chloride

Question 94

Fill in the fllowing chart for signs and symptoms accompanying the pathophysiological processes in metabolic alkalosis:

Answer 94

Question 95

What are 4 serious complications of metabolic alkalosis?

Answer 95

1. Neurological –> tetany/seizures/decreased mental status
2. Decreased coronary blood flow –> arrhythmias
3. Hypoventilation –> hypoxemia
4. Increased ammonia production –> hepatic encephalopathy

Question 96

How do you treat metabolic alkalosis? (6)

Answer 96

1. Correct the cause
2. Correct the deficiency (Cl-, water, K+, etc.)
3. Expand ECF volume with normal saline if appropriate
4. RAAS blockade
5. O2 if necessary
   (6. Rarely –> HCl infusion, aetazolamide, oral lysine HCl)

Question 97

What is respiratory acidosis? What is the differene between acute and chronic?

Answer 97

A failure of the respiratory system leading to a blood pH <7.35

Acute = PaCO2 > 45 with acidemia

Chronic = PaCO2 > 45 with near normal pH and serum HCO3- >30 (renal compensation)

Question 98

What are causes of acute respiratory acidosis?

Answer 98

Brainstem = stroke, meds/drugs

Neuromuscular = myasthenia gravis, trauma, ALS, G-B syndrome, muscular dystrophy

Airway obstruction = foreign object, asthma

Impaired gas exchange at alveoli:capillary = COPD, pneumonia, pulmonary edema

Question 99

What are causes of chronic respiratory acidosis? (4)

Answer 99

COPD

Pickwickian syndrome

Interstitial Lung Disease

Thoracic deformities

Question 100

How does the body compensate for respiratory acidosis? (3)

Answer 100

1. Respiratory centers respond to baroreceptors and increase rate and depth of breathing
2. Cellular buffering causes a 1 mEq/L HCO3- increase for every 10mmHg increase in PaCO2

3 Renal compensation causes a 3.5 mEq/L HCO3- increase for every 10mmHg increase in PaCO2 (increased bicarb reabsorption and production, renal excretion of carbonic acid)

Question 101

What are some signs and symptoms of a respiratory acidosis?

Answer 101

1. Headache
2. Anxiety
3. Blurred vision
4. Restlessness
5. Confusion

Question 102

How is acute respiratory acidosis treated?

How is chronic respiratory acidosis treated?

Answer 102

Acute = address underlying cause and use artificial ventilation if needed

Chronic = manage underlying condition, give antibiotics/diuretics/bronchodilators/corticosteroids as needed, artificial ventilation if needed

Question 103

What is respiratory alkalosis? What is the difference between acute and chronic?

Answer 103

Failure of the respiratory system leading to a blood pH of >7.45

Acute = low CO2 and high pH

Chronic = low CO2 and normal pH (renal compensation)

Question 104

What are some causes for respiratory alkalosis? (9)

Answer 104

Respiratory center

• Normal response to hypoxia (pneumonia, PE, high altitude)
• Abnormal response to hypoxia (panic attack, OD on ASA)
• Brainstem disorders irritating center (tumor)

Iatrogenic increased respiration

• Wrong settings on a mechanical ventilator

Other causes

• Heart disorder
• Thermal insult
• Fever
• Compensation for volume loss in vocal cord paralysis
• Liver disease

Question 105

How does the body compensate for respiratory alkalosis?

Answer 105

1. Respiratory center senses low CO2 levels and responds by slowing down minute ventilation
2. Cellular buffering causes 2 mEq/L HCO3- decrease for every 10 mmHg decrease in PaCO2 (proteins in cells excrete H+ into blood –> ex. Hb)
3. Renal compensation causes 4-5 mEq/L HCO3- decrease for every 10 mmHg decrase in PaCO2 (release of more HCO3- into blood at the PCT)

Question 106

What are some signs and symptoms of respiratory alkalosis?

Answer 106

• Dizziness/light-headedness
• Bloating
• Numbness and muscle spasms in hands and feet
• Arm tingling
• Chest discomfort, heart palpitations
• Confusion
• Dry mouth
• SOB

Question 107

How is respiratory alkalosis treated?

Answer 107

1. Treat the underlying cause
2. ABG monitoring
3. Paper bag breathing
4. Pursed lip breathing

Question 108

What [K+] is considered hyperkalemia? Hypokalemia?

Answer 108

Hyperkalemia = [K+] > 5.5 mmol/L

Hypokalemia = [K+] < 3.5 mmol/L

Question 109

What are characteristics of an ECG in:

• Hyperkalemia?
• Hypokalemia

Answer 109

Hyperkalemia = peak T waves –> widening QRS complex –> absence o P waves –> sine waves –> asystole, ventricular fibrillation

Hypokalemia = T and U wave (biphasic T), prolonged QT interval, tachycardia

Question 110

What are 3 complications of hyperkalemia?

What are 7 complications of hypokalemia?

Answer 110

Hyperkalemia:

1. Arrhythmias
2. Muscle weakness/spasms
3. Paralysis

Hypokalemia:

1. Arrhythmias
2. Weakness/fatigue
3. Muscle cramps
4. Paralysis
5. Rhabdomyolysis
6. Polyuria from ADH inhibition
7. Interstitial fibrosis

Question 111

How do you treat hypokalemia?

Answer 111

1. Replace potassium (KCl- a good cohice; KHCO3- good if there is acidosis, do NOT give glucose, ensure there is enough Mg)
2. Give calcium to eliminate arrhythmias
3. Treat the underlying cause

Question 112

How do you treat hyperkalemia?

Answer 112

1. Remove the excess K+
   - Renal = Non-K+ sparing diuretic
   - GI = resins (binds K+) or induction of diarrhea
   - Shift (glucose, beta agonist, bicarbonate)
   - Dialysis in extreme cases
2. Give calcium to eliminate arrhythmias
3. Treat the underlying cause

Question 113

What is shock from a medical standpoint?

Answer 113

A life threatening condition occurring when the body does not get enough blood flow

Question 114

What are 4 main categories of shock?

Answer 114

1. Cardiogenic –> due to heart problems
2. Hypovolemic –> due to low total blood volume
3. Obstructive –> due to blood flow obstruction outside the heart
4. Distributive –> due to abnormal fluid distribution

Question 115

What are 4 types of distributive shock?

Answer 115

1. Anaphylactic
2. Septic
3. Neurogenic
4. Endocrine

Question 116

What is sepsis?

What is septic shock?

Answer 116

Sepsis = organ injury/damage in response to infection; leads to low BP and abnormal cellular metabolism

Septic shock = worsened sepsis to the point where BP cannot be maintained with IV fluids alone

Question 117

What are common infections that are known to lead to septic shock? (10)

What percentage of septic shock is due to UTI? RTI? IV? Idiopathic?

Answer 117

• Appendicitis
• Pneumonia
• Bacteremia
• Diverticulitis
• Pyelonephritis
• Meningitis
• Pancreatitis
• Necrotizing fasciitis
• MSRA
• Mesenteric ischemia

UTI = 35%; RTI = 15%, IV = 15%, iatrogenic = 30+%

Question 118

What is the name for toxins secreted by:

1. Gram-positive bacteria
2. Gram-negative bacteria

Answer 118

1. Exotoxins, enterotoxins
2. Endotoxins, lipopolysaccharides

Question 119

Why does vasodilation occur in septic shock? (3)

Answer 119

1. Toxins from bacteria cause direct endothelial injury and thus release of the vasodilator NO
2. Toxins from bacteria activate the complement pathway which activates mast cells to release the vasodilator histamine
3. Toxins from bacteria activate immune cells (macrophages/neutrophils) which release cytokines leading to vasodilation

Question 120

Why does septic shock lead to decreased BP?

Answer 120

1. Extreme systemic vasodilation
2. Immune response causes leaky vessels which decreases intravascular volume
3. Immune response causes endothelial damage which leads to clots

Question 121

In septic shock, what does “low BP” mean?

Answer 121

SBP <90 mmHg

MAP <70 mmHg

SBP decreasing 40 mmHg or more without another cause

Question 122

What are signs of end-organ dysfunction? (4)

Answer 122

1. Kidney failure
2. Liver dysfunction
3. Changes in mental status
4. Elevated serum lactate

Question 123

What are symptoms of infection in SIRS?

Answer 123

1. Fever (>38.0decC) or hypothermia (<36.0degC)
2. Hyperventilaion (>20 bpm or PaCO2 <32mmHg)
3. WBC < 4,000 cells/mm^3 or >12,000 cells/mm^3
4. Tachycardia with HR > 90bpm

Question 124

How is septic shock treated? (6)

Answer 124

1. Give IV fluids (with albumin if large volume)
2. Administer a broad spectrum antibiotic
3. Administer vasopressors (NE + possibly Epi; angiotensin II in adults)
4. Identify source and attempt to control it
5. Support any major organ dysfunction (ex. dialysis)
6. Get high fever under control

Question 125

What is acute kidney injury?

What are the 3 categories of AKI?

Answer 125

Acute and sustained decrease in renal function causing either

1. Increased serum creatinine by 44.2 umol/L
2. Increase in serum creatinine by 20%

3 categories:

Prerenal = decreased renal perfusion; preserved tissue integrity

Renal = injury to the structures of the nephron

Postrenal = obstruction of collecting system

Question 126

What are t

Question 127

AKI epidemiology

1. How many adults per year have AKI with a serum creatinine > 500 uM?
2. How many adults per million have AKI with a serum creatinine > 300 uM?
3. How many adults per million have renal replacement therapy a year due to AKI?
4. What % of AKI is initially pre-renal?
5. What 3 populations have increased risk for post-renal AKI?

Answer 127

1. 172 million
2. ~550/million
3. 131/million
4. 75%
5. Prostatic disease, single kidneys, intra-abdominal/pelvic cancer

Question 128

What are 4 categories of causes for pre-renal AKI? Please list examples in each category.

Answer 128

1. Absolute fluid loss
   - Ex. Major hemorrhage, vomiting, diarrhea, sever burns
2. Relative fluid loss
   - Ex,. Distributive shock, CHF, decompensated liver cirrhosis
3. Local artery problems
   - Ex. Renal artery stenosis, embolus, extrinsic compressionm, vasculitis
4. Exogenous cause
   - Ex. NSAIDs, ACEI or ARBs in context of CHF, RAS, dehydration

Question 129

What are 6 pathophysiological consequences that occur in pre-renal AKI?

Answer 129

1. Azotemia
2. Oliguria
3. Edema
4. Hypernatremia
5. Hypertension
6. Progression to ischemic acute tubular necrosis

Question 130

What are 3 categories of causes for post-renal AKI? Please list examples in each category.

Answer 130

1. Extrinsic compression
   - Ex. Intra-abdominal tumor, prostatic tumor, BPH
2. Internal blockage
   - Ex. Kidney stones, bladder stones, tumor inside the tract
3. Exogenous cause
   - Ex. Obstructed urinary catheter

Question 131

What are 6 pathophysiological consequences that occur in post-renal AKI?

Answer 131

1. Oliguira
2. Azotemia
3. Hydronephrosis
4. Edema from pressure
5. Hypernatremia from pressure –> becoming hyponatremia as high pressures damage the lumen epithelium
6. Hyperkalemia (on complete obstruction)

Question 132

What are the 4 types of renal AKI?

Answer 132

1. Vascular
2. Glomerular
3. Interstitial
4. Tubular necrosis

Question 133

What are causes of AKI?

Vascular (2)

Glomerular (3)

Interstitial (5)

Tubular necrosis (3)

Answer 133

1. Vascular
   - Microangiopathies (pre-eclampsia, DIC, vasculitis, HT), sickle cell disease
2. Glomerular
   - Post-infectious glomerular nephritis, nephrotic syndrome, auto-immune destruction
3. Interstitial
   - Drugs, chronic use of analgesics, DM, pyelonephritis, auto-immune destruction
4. Tubular necrosis
   - Ischemia (pre-renal AKI), exogenous toxins (drugs, poisons), endogenous toxins (rhabdomyolysis, hemolysis, tumor lysis syndrome, oxalate, myeloma)

Question 134

Describe the pathophysiology of tubular necrosis:

Answer 134

1. Something causes necrosis of the tubular epithelium
2. Dead epithelial cells slough into the tubule and build up, plugging the tubule
3. This increases tubular pressure proximal the plug –> decreased GFR –> oliguria and azotemia
4. This decreases tubular pressure distal to the plug –> RAAS –> edema, hypernatremia
5. With more and more damage, less re-absorption and secretion occurs –> hyperkalemia, metabolic acidosis

Question 135

Describe the pathophysiology of glomerulonephritis:

Answer 135

1. Antigen-antibody complexes deposit in glomerular tissue
2. This activates teh complement system which recruits more immune cells such as macrophages and neutrophils
3. Immune cells release lysosomal enzymes which causes inflammation and damage of the podocytes
4. Damaged podocytes allow protein tino the urine –> proteinura, hematuria
5. Fluid leakage reduces pressure gradient driving filtration of the smaller molecules ane electrolytes and GFR actually goes down –> oliguira, azotemia
6. The kidneys try to respond by activating RAAS –> hypertension, hypernatremia, edema

Question 136

Fill in the following findings for pre-renal, renal, and post-renal AKI:

Answer 136

Question 137

When is renal biopsy indicated in AKI? (4)

Answer 137

1. Unexplained with 2 non-obstructed normal sized kidneys
2. AKI in the presence of nephritic syndrome
3. Systemic disease associated AKI
4. Kidney transplant dysfunction

Question 138

What is the first line imaging modality in AKI? What is used for F/U?

Answer 138

First line = renal U/S

F/U = MRI and CT (without contrast)

Question 139

What post void residual value would suggest neurogenic bladder dysfunction?

Answer 139

>50-100mL

Question 140

What are all the steps taken when managing/treating AKI?

Answer 140

1. Prevent cardiovascular collapse/death and call a nephrologist
2. Identify the underlying cause and try to treat
3. Correct electrolyte imbalance
4. Monitor kidney function

(Avoid NSAIDs, iodinated contrasts, some antibiotics)

Question 141

What 7 groups are at risk for acute tubular necrosis as a post-surgical complication?

Answer 141

1. Pre-existing renal impairment
2. Hypertension
3. Cardiac disease
4. Peripheal vascular disease
5. DM
6. Jaundice
7. Advanced age

Question 142

What 2 drug categories are most frequently associated with drug-induced AIN?

Give 7 other examples:

Answer 142

1. NSAIDs
2. PPIs

Others =

1. Cephalosporins
2. Methicillins
3. Fluoroquinolones
4. Phenytoin
5. Allopurinal
6. 5-aminosalicylates
7. Captopril

Question 143

What are 4 theories for how drugs cause AIN via immune reactions?

Answer 143

1. Drug serves as a hapten –> binds to endogenous protein making it antigenic
2. Molecular mimicry
3. Drugs become trapped in interstitium
4. Drugs form a circulating immune complex which is deposited in the interstitium

Question 144

What type of immune reaction is drug-induced AIN thought to be?

(2 possible types…cell vs. antibody)

Answer 144

Type I (IGgE) or IV (T cell) hypersensitivity

Cell-mediated immunity

Question 145

What is a compliation of drug-induced AIN?

Answer 145

Scar tissue that permanently damages renal function

Question 146

What are 6 presenting symptoms indicative of drug-induced AIN?

What are some other more general symptoms?

On U/S, what happens to echogenicity?

Answer 146

1. Sudden impairment of renal function
2. Mild proteinuria (not nephrotic)
3. Abnormal urinalysis (hematuria, pyuria, leukocyte casts, eosinophils, leukocytes)
4. Flank pain
5. Normal BP
6. No edema

General = malaise, anorexia, nausea, joint pain, skin rash

Echogenicity increases on U/S

Question 147

How is drug-induced AIN diagnosed?

Answer 147

Must be confirmed with a kidney biopsy

• Dziffuse or patchy inflammatory infiltrates in the deep cortex and outer medulla
• Mostly T-cells, monocytes, and macrophages
• Few plasma cells, eosinophils, neutrophils
• Sparse, non-necrotic granulomas
• Possible tubulitis
• Interstitial edema between tubules
• Normal glomeruli

Question 148

How is drug-induced AIN treated?

Answer 148

1. Identification and withdrawal of the allergen
2. Early treatment with corticosteroids for the first 5 days (prednisone)
   - This is controversial

Question 149

What are 6 indications for renal biopsy?

Answer 149

1. Isolated/persistent hematuria
   - Thought to come from glomerulus
   - Combined with features of progressive renal disease
2. Prtoteinuria at high or increasing levels
3. AKI when cause is unknown or thought to be acute nephritic syndrome
4. Tumors
5. Transplant
6. Query connective tissue disease

Question 150

What are contraindications for renal biopsy?

Absolute (5)

Relative (9)

Answer 150

Absolute = bleeding diathesis, uncontrolled HTN, active renal infection, small kidneys, no consent

Relative = solitary kidney, azotemia, uremia, anatomical abnormalities, polycystic, on anti-clotting meds, pregnancy, UTI, obesity

Question 151

What are 6 risks associated with renal biopsy?

Answer 151

1. Bleeding –> shock/anemia/transfusion risks/death
2. Infection
3. Damage to surrounding structures (bowel and bladder)
4. Only getting scar tissue and needing to re-biopsy
5. Allergies to materials used
6. Formation of AV fistula

Question 152

What is diabetic nephropathy? What values are used to evaluat it?

Answer 152

Chronic loss of kidney function occurring in those with DM

Evaluated via urine albumin excretion or reduction in GFR

Question 153

1. What % of those with DM type I will experience diabetic kidney disease?
2. What % of DM type I deaths are due to diabetic kidney disease
3. What % of those with DM type II will experience diabetic kidney disease?
4. What % of DM type II deaths are due to diabetic kidney disease

Answer 153

1. 15-40%
2. 21%
3. 5-20%
4. 11%

Question 154

What factors increase the risk and rate of acquiring diabetic kidney disease in those diagnosed with DM? (4)

Answer 154

1. Poorly controlled hyperglycemia (A1C >7.5%)
2. Poorly controlled high BP (>130/80)
3. Smoking
4. Family history

Question 155

What is the general overview of the pathology behind diabetic kidney disease? (non-enzymatic glycosylation)

Answer 155

1. Narrowing efferent arteriole from vessel glycation (hyaline arteriosclerosis) causes increased pressure in the glomerulus
2. In response to increased glomerular pressure there is afferent arteriole dilation and mesangial ECM expansion –> thickened basemenet membrane
3. The basement membrane thickening stretches out the podocytes, which allows proteins to slip into the urine
4. Overall there is hyperfiltration
5. Over time, the increased pressure causes tissue injury which develops into fibrosis.
6. Fibrosis leads to decreased filtration and proteins, creatinine, water, etc. build up in the blood
7. Kidney function declines into CKD and eventual ESRD

Question 156

Explain the process of non-enzymatic glycosylation and how it leads to diabetic nephropathy:

Question 157

Other than non-enzymatic glycoslyation, briefly outline other ways that diabetes contributes to kidney injury. (6)

Answer 157

1. Sorbitol pathway –> ROS and decreased anti-oxidant capacity –> cellular damage
2. Sorbitol pathway –> osmotic stress –> cellular damage
3. Diacylglycerol pathway –> increased transcription of ECM, fibronectin, collagen –> fibrosis
4. Hypoxia from increased metabolism –> HIF-1 activtaion –> collagen and fibtronectin production –> fibrosis
5. Decreased NO production
6. Increased prerenin receptors on podocytes in the presence of hyperglycemia –> more activation of RAAS

Question 158

Explain the findings in GFR and proteinuria over the course of diabetic kidney disease:

Answer 158

Question 159

What are 9 symptoms of diabetic nephropathy? Why do they occur (brief explanation).

Answer 159

1. Nocturia and frequent day time urination (during hyperfiltration stage)
2. Foamy urine (from proteinuria)
3. Tiredness (from hypoalbuminemia and uremia)
4. Headaches (from increased systemic BP)
5. Nausea and vomtigin (from uremia)
6. Lack of appetite (secondary to nausea and vomiting)
7. Uremic frost (from urea depositing in skin)
8. Itchy skin (from urea collecting in the skin)
9. Leg swelling (from hypoalbuminemia, RAAS)

Question 160

What are some end stage complications of diabetic nephropathy? (8 categories)

Answer 160

1. Uremia –> lethargy, pericarditis, encephalopathy
2. Decreased Epo –> anemia
3. Iron deficiences –> anemia, inflammation, bone marrow suppression
4. Fluid retention –> pulmonary edema
5. Hyperphosphatemia –> vascular calcification
6. Hyperkalemia –> muscle cramps, cardiac arrhythmias
7. Decreased calcitriol and vitamin D –> hyperparathyrodisim, vascular calcification, osteodystrophy
8. Metabolic acidosis

Question 161

How is diabetic nephropathy prevented?

How is it “treated”?

Answer 161

1. Screening = yearly (wait 5 years after diagnosis for type I)
2. Hypertensive medications (ACEI, ARB, vasopressor, Ca++ channel blocker)
3. Dyslipidemia medication (statins)
4. Hyperglycemic medications (sulphonylureas, glitazones, SGLT2 inhibitors, DPP4-inhibitors, GLP-1s, metformin)

The closest thing to treatment is renal replacement therapy (transplant or dialysis)

Question 162

Define chronic kidney disease:

Answer 162

A group of disorders affecting the structure and function of the kidney and causing a decline in glomerular filtration rate and irreversible loss of nephrons over 3+ months

Question 163

What is the diagnostic criteria for CKD? (2)

Answer 163

1. Kidney damage for 3+ months (structural/functional abnormalities of the kidney) with or without decreased GFR
2. GFR <60 mL/min/1.73m^2 for 3+ months with or without kidney damage

Question 164

What is the GFR for the following CKD stages:

G1, G2, G3a, G3b, G4, G5

What is the albuminuria for the following CKD stages:

A1, A2, A3

Answer 164

G1 = 90+

G2 = 60-89

G3a = 45-59

G3b = 30-44

G4 = 15-29

G5 = <15

A1 = <30 mg/g

A2 = 30-300 mg/g

A3 = >300 mg/g

Question 165

What health conditions are at increased risk of CKD? (6)

Answer 165

Diabetes

Hypertension

Obesity

High cholesterol

Lupus

Cardiovascular disease

Previous episode of AKI

Structural abnormalities of the urinary tract

(Family history)

Question 166

What races are at increased risk of CKD? (4)

Answer 166

African Americans (Apo-1 mutation)

Indigenous Peoples

Hispanics (sugar cane workers)

South Asians (Pakistan, Sri Lanka, Bangladesh, India)

Question 167

What are the 4 categories of causes of CKD?

Answer 167

1. Vascular
2. Glomerula
3. Tubulointerstitial
4. Cystic (PCKD)

Question 168

What are 5 vascular causes of CKD?

Answer 168

1. Renal artery stenosis from FSGS
2. Renal artery atherosclerosis
3. Hypertension
4. Vasculitis
5. Microangiopathy

Question 169

What are 7 glomerular causes of CKD?

Answer 169

1. Primary nephritis from IgA
2. Autoimmune disease
3. Connective tissue disease
4. Malignant disease
5. Drugs (NSAIDs, tobacco)
6. Hyperfiltration
7. Systemic infection

Question 170

What are 7 tubulointerstitial causes of CKD?

Answer 170

1. Autoimmune disease
2. Connective tissue disease
3. Granulomatous disease
4. Drugs
5. Obstructive nephropathy
6. Chronic infection
7. Post-AKI

Question 171

How does hypertension cause CKD?

Answer 171

1. High pressure causes thickening of all arteries to withstand the pressure, including the afferent arteriole
2. Narrowed afferent lets less blood into the glomerulus
3. Less blood causes ischemic injury
4. Immune cells respond to the injury and release TGF-beta
5. TGF-beta causes mesangial cells to regress to mesangioblasts which secrete ECM. This ECM causes glomerulosclerosis
6. The more nephrons that are lost, the higher the GFR gets in remaining nephrons
7. Overtime more and more nephrons are lost until there is complete failure.

Question 172

What are the physiological consequences of CKD?

Answer 172

1. Oliguria
2. Azotemia
3. Hyperkalemia
4. Hyperphosphatemia
5. RAAS activation
6. Hypocalcemia
7. Anemia
8. Metabolic acidosis

Question 173

What are 3 causes for hyperkalemia in CKD?

Answer 173

1. Decreased secretion of sodium in the tubule due to cellular damage and lowered GFR
2. RAAS activation
3. Metabolic acidosis

Question 174

What is the presentation of azotemia? (8)

Answer 174

1. Nausea/vomiting, loss of appetite
2. Hiccoughs, cramps (neuro)
3. Encephalopathy/asterixis/coma/death
4. Pericarditis
5. Increased risk of bleeding
6. Uremic frost
7. Amenorrhea from decreased estrogen
8. Impotence from decreased testosterone

Question 175

What 4 things are investigated during CKD?

Answer 175

1. GFR
2. Albuminemia
3. Kidney biopsy
4. Renal U/S

Question 176

What are 4 serious complications of CKD?

Answer 176

1. Anemia of chronic kidney disease (from decreased production of Epo)
2. Secondary hyperthyroidism and bone marrow disease due to elevated phosphorous and low calcium stimulating PTH
3. Volume overload causing pulmonary edema
4. Metabolic acidosis

Question 177

What “treatment” is available for CKD?

Answer 177

1. Prevention of progression (statins, aspirin, ACEI, ARB, oral DM meds, low protein diet)
2. Immunosuppression (corticosteroids/cyclophosphamide) when relevant
3. Ferrous gluconate for anemia
4. Dialysis
5. Renal transplant

Question 178

What does a CKD diet look like? (9 things)

Answer 178

1. Adequate calories to maintain weight (and not lose)
2. Low protein diet (ex. carbs, fruit, veggies)
3. Low fat/unsat fat diet (ex. olive/peanut/corn oils)
4. Only “healthy” carbs low in K+ and P(3-)
5. Low sodium (fresh food, no pickles/condiments)
6. Low potassium (apples, cauliflower, white bread, beef, chicken)
7. Low phosphorous (Italian bread, corn, light soda)
8. Limited fluids (less soup, ice cream, watery fruits/veggies)
9. Supplements (vitamin D, water-soluble vitamins)

Question 179

What are the upper limits for potassium, sodium, phosphorous, and protein in a CKD diet?

Answer 179

Question 180

Compare peritoneal and hemo dialysis:

Answer 180

Question 181

Define dialysis and give 3 situations in which it is indicated:

Answer 181

Process of removing excess water, solutes, and toxins from the blood in those whose native kidneys can’t do this naturally

AKI, CKD stage 5, ESRD

Question 182

What are 3 ways to access the blood in hemodialysis?

Answer 182

1. Primary arteriovenous fistula (usually lower arm)
2. Synthetic bridge graft
3. Central venous catheter (dialysis line)

Question 183

What are the indications in AKI that dialysis is needed? (6)

Answer 183

A = acidemia unresponsive to meds

E = electrolyte abnormalities unresponsive to meds

I = intoxication (salicylic acid, lithium, isopropanol, Mg+ laxatives, ethylene glycol)

O = fluid overload unresponsive to diuretics

U = uremia complications (pericarditis, encephalopathy, GI bleeding)

BUN > 80-100 mg/dL

Question 184

What are the indications in AKI that dialysis is needed? (10)

Answer 184

1-5 = AEIOU

6. Refractory accelerated hypertension
7. Persistent severe nausea/vomiting
8. Creatinine clearance <7-10 mL/min
9. BUN > 36 mM
10. Heart concerns

Question 185

What are some absolute contraindications for peritoneal dialysis? (8)

Answer 185

1. Type II ultrafiltration failure
2. Severe IBD
3. Acute active diverticulitis
4. Abdominal abscess
5. Active ischemic bowel disease
6. Severe active psychotic disorder
7. Marked intellectually disability
8. Third trimester of pregnancy

Question 186

What are some relative contraindications for peritoneal dialysis? (8)

Answer 186

1. Severe malnutrition
2. Multiple abdominal adhesions
3. Infection
4. Proteinuria > 10g/day
5. Demenita
6. Physical barriers (amputation, obesity, blindness, homeless)
7. Depression
8. Ostomy

Question 187

What are some absolute contraindications for hemodialysis? (2)

Answer 187

1. Unconsenting/uncooperative patient
2. Hemodynamically unstable patient

Question 188

What necessitates amputations in many diabetics?

Answer 188

1. Peripheral artery disease –> reduced blodo flow –> reduced healing
2. Neuropathy –> reduced feeling –> undetected wounds
3. Skin changes –> skin breaks more easily

Together this causes damage that persists until gangrene and osteomyelitis occurs

Question 189

What are 7 complications post-amputation?

Answer 189

1. Hematoma
2. Phantom limb sensation/pain
3. Re-perfusion injury
4. Sepsis
5. Failure to heal
6. Depression
7. DVT

Question 190

Fill in the following chart regarding steroid hormone synthesis:

Answer 190

Question 191

What is congenital adrenal hyperplasia? (CAH)

Answer 191

A group of autosomal recessive disorders involving a deficiency of an enzyme involved in the synthesis of cortisol, aldosterone, and androgens.

Question 192

Fill in the following chart regarding four different types of congenital adrenal hyperplasia:

Answer 192

Question 193

What is the prevalence of CAH in the general global population?

What 2 populations are at increased risk of classic CAH?

What 2 populations are at increased risk of non-classic/mild CAH?

Answer 193

General = 1/15,000

Classic = Yupic Eskimos of Alaska, French Island of La Reunion

Non-classic/Mild = Hispanic, Ashkenazi Jews

Question 194

What is the difference between classic, simple, and non-classic CAH?

Answer 194

Classic = severe form

Simple = mild form

Non-classic = very mild form

Question 195

What types of CAH lead to excess androgen? (2)

What is the presentation in someone with excess androgen?

• Males (2), Females (6), Both (5)

Answer 195

21-hydroxylase and 11-beta hydroxylase deficiencies

Males

• Functional penis but without sperm
• Normal to enlarged penis

Females

• Ambiguous genitalia
• Menstrual irregularity in adolescence
• Infertility due to anovulation
• Clitoromegaly
• Shallow vagina
• Hirsutism

Both

• Early pubic hair
• Rapid growth in childhood
• Precocious puberty or sexual infantilism
• Excessive facial hair
• Accelerated linear growth and skeletal maturation

Question 196

What types of CAH lead to insufficient androgen/estrogen? (2)

What is the presentation in someone with insufficient androgen/estrogen?

• Males (2), Females (4)

Answer 196

17-alpha hydroxylase and 3-beta hydroxysteroid dehydrogenase deficiency

Males

• Undervirilization
• Apparently female external genitalia

Females

• Sexual infantilism or abnormal pubertal development
• Infertility
• Amenorrhea
• Lack of breast development

Question 197

What types of CAH lead to excessive mineralocorticoids? (2)

What is the presentation in someone with excessive mineralocortiocids? (7)

Answer 197

17-alpha hydroxylase and 11-beta hydroxylase deficiency

• Sodium retention (volume overload and edema, hypertension, CV complications)
• Hypokalemia
• Metabolic alkalosis
• Decreased adult height

Question 198

What types of CAH lead to insufficient mineralocorticoids? (2)

What is the presentation in someone with insufficient mineralocortiocids? (7)

Answer 198

3-beta HSD, 21-alpha hydroxylase deficiency

• Hyponatremia (vomiting, hypotension, hyperkalemia, dehydration, death)
• Hyperpigmentation of genitalia and areolae

Question 199

What are the lab investigations in CAH?

Answer 199

Question 200

What types of imaging are done in CAH?

Answer 200

1. CT scanning to exclude bilateral adrenal hemorrhage (acute onset)
2. Pelvic U/S to identify uterine or renal anomalies (ambiguous genitalia)
3. Urogenitography to define the anatomy of the internal genitalia
4. Bone-age study to evalue advanced skeletal maturation (precocious pubic hair, clitoromegaly, accelerated growth)

Question 201

What are 5 complications of CAH?

Answer 201

1. Salt-wasting –> morbidity from hyponatremia, hyperkalemia, dehydration, and hypotension
   - Concerning in males with 21-alpha hydroxylase whose external genitalia look ~normal
2. Lack of GCs during illness/trauma/surgery –> morbidity
3. Increased viral infection susceptibility
4. Short stature
5. Infertility

Question 202

How is CAH treated/managed?

Answer 202

1. IV bolus of isotonic NaCl if there is hyponatremia and dehydration
2. Stress dosage of hydrocortisone every 6 hours
3. Dextrose in rehydration fluid if there is hypoglycemia
4. ST GC therapy for MC deficiency
5. LT GC and MC therapy for GC and MC replacement
6. Androgen suppression if there is excess androgens
7. Exogenous testosterone and/or estrogen if there is insufficient androgens
8. Surgery for clitoral recession and vaginoplasty

(Dexamethasone is used in CAH female fetuses but doesn’t treat the condition and may cause cognitive behavioural defects)

Question 203

What is androgen insensitivity syndrome?

What are the 3 types?

Answer 203

An X-linked recessive condition resulting in a failure of normal masculinization of the external genitalia in XY individuals; an intersex condition

1. Complete = normal extermal female genitalia
2. Partial = ranges from mildly virilized female to mildly undervirilized male external genitalia
3. Mild

Question 204

What is the internal sexual organs in Androgen Insensitivity Syndrome?

Answer 204

Testes present but undescended (SRY still present)

Improper epididymis, vas deferens, and seminal vesicles (testosterone can’t act on Wolffian ducts properly)

No fallopian tubes, uterus, or upper vagina (anti-Mullerian hormone still present)

Question 205

What is the overall prevalence of AIS?

What is the incidence of CAIS? PAIS?

Answer 205

AIS = 1/20,400

CAIS = 1/99,000

PAIS = 1/130,000

Question 206

What causes androgen-insensitivity syndrome?

Answer 206

Loss of function mutation in the androgen receptor gene

• Multiple different possible mutations, either complete deletion, partial deletion, point mutation, or small insertion

Question 207

What is the presentation of complete androgen-insensitivity syndrome?

Answer 207

Female genitalia

Lack of pubic or axiallyar hair

Lack of acne

Absence of voice change

Low bone mineral density

Infertility

Female secondary sex characterisitcs

Reduced clitoral length

Possible inguinal masses (which are the undescended testes)

Question 208

What is Kennedy Disease?

Answer 208

A motor neuron disease caused by a CAG expansion in the androgen receptor gene; leads to spinal and bulbar muscular atrophy, post-pubertal gynecomastia, reduced fertility, possible sensory deficits, and decreased facial hair growth

Question 209

What are possible investigations in the work up for androgen-insensitivity syndrome

Answer 209

1. Karyotype
2. FISH probles for the SRY region of the Y chromosome
3. Testosterone and DHT levels (expect high)
4. Mutation analysis of AR
5. Pelvic U/S to identify Wolffian or Mullerian structures
6. Histology of the testes (biopsy)

Question 210

What are 4 complicat ions associated with androgen-insensitivity syndrome?

Answer 210

1. Increased risk of tesitcular malignancy if testes are not removed (CAIS)
2. Increased risk of germ cell tumors if testes are not removed (PAIS)
3. Pyschological morbidity
4. Osteoporosis

Question 211

What are the 3 main categories of treatment for androgen-insensitivity syndrome? Give examples of each.

Answer 211

1. Surgery - orchidectomy, vaginal lengthening, cosmetic reconstructive
2. Hormone replacement therapy - estrogen replacement is CAIS, estrogen or testosterone/DHT replacement in PAIS
3. Psychological support (parental genetic counseling, pediatric psychologists, AIS support groups)

Question 212

What are 6 different cultures that practice consanguinity?

Answer 212

1. North African
2. West Asian
3. South Indian
4. Pakistan
5. Turkey
6. Lebanon

Question 213

What is precocious pubrerty? What are the two main categories?

Answer 213

Progression through the Tanner Scale before 95% of children that age.

1. Central/Gonadotropin-dependent = abnormality located in the brain
2. Peripheral/Gonadotropin-independent = abnormality located in the gonads or adrenal glands

Question 214

What are 5 causes of central / gonadotropin-dependent precocious puberty?

Answer 214

1. Brain tumor (hypothalamic hamartoma, langerhans cell histiocytosis, hCG releasing tumor)
2. Prior infection (CNS TB)
3. Brain trauma (radiation, injury, hydrocephalus)
4. Brain abnormalities
5. Idiopathic

Question 215

What are 5 causes of peripheral / gonadotropin-independent precocious puberty?

Answer 215

1. Tumors and cysts (Sertoli-Leydig, Granulosa-Theca tumors, germ cell tumors)
2. Genetics (McCune Albright, FMPP, aromatase excess, 21/11beta-OH-deficiency)
3. Hypothyroidism (Van Wyk and Grumbach syndrome)
4. Environmental exogenous hormoens
5. Iatrogenic meds/creams containing sex hormones

Question 216

What are 4 possible investigations to order for the presentation of precocious puberty?

Answer 216

1. GnRH agonist stimulation test (done first)
   - Increased FSH/LH = central cause
   - Normal FSH/LH = peripheral cause
2. Blood tests (elevated or normal LH/FSH)
3. Imaging with U/S or MRI of the brain/gonads (tumors, size, cysts, abnormalities)
4. Bone Age X-Ray

Question 217

What are 6 complications (including increased risks) associated with precocious puberty

Answer 217

1. Early fusion of epiphyses leading to reduced final stature
2. Slipped capiital femoral epiphysis
3. Increased risk of sexual abuse
4. Pscyhological damage
5. Increased risk of breast cancer in females
6. Increased aggressiveness in males

Question 218

What are the 3 treatment options for precocious puberty?

Answer 218

1. GnRH analogues to over-express GnRH, effecgively suppressing LH and FSH –> used for central causes
2. Antagonists to estrogen or testosterone –> used for peripheral causes
3. Sugery to remove any cysts or tumors

Question 219

What is delayed puberty?

What are the 3 different categories?

Answer 219

Lack of progression through the Tanner scale by the time 95% of children that age have begun to sexually mature (post 13 in females and post 14 in males)

1. Primary hypogonadism / hypergonadotropin hypogonadism = decreased sex steroids due to a gonadal dysfunction
2. Secondary hypogonadism / hypogonadotropin hypogonadism = decreased sex steroids due to a brain dysfunction
3. Constitutional delay = a natural non-pathologic delay

Question 220

What are 5 acquired and 5 congenital causes of hypergonadotropin hypogonadism?

Answer 220

Acquired:

1. Radiation
2. Chemotherapy
3. Physical trauma to the gonads
4. Surgery
5. Infection

Congenital

1. Klinefelter syndrome
2. Turner syndrome
3. Noonan syndrome
4. XY with SRY gene-immunity
5. Autoimune disorders

Question 221

What are 8 acquired and 2 congenital causes of hyporgonadotropin hypogonadism?

Answer 221

Acquired:

1. Radiation
2. Chemotherapy
3. Physical trauma to the brain
4. Tumor causing decreased GnRH, prolactinoma, or hyperthyroidism
5. Excess exercise
6. Malnutrition
7. Obesity
8. Stress
   (9. Chronic illness)

Congenital:

1. Kallman syndrome
2. Panhypopituitarism
   (3. Chronic illness)

Question 222

What are 5 possible investigations to complete in the work up for delayed puberty?

Answer 222

1. Bone age X-ray
2. GnRH agonist stimulatory test
3. Medical and family history
4. Imaging using U/S or MRI of the brain and gonads (abnormalities, trauma, tumors, etc.)
5. Physical exam to examine development

Question 223

What are 3 treatments/ managements in delayed puberty?

Answer 223

1. Hormone replacemen therapy
2. Surgery to remove a tumor
3. Infertility treatment to make reproduction possible if appropriate

Question 224

What is skewed X-inactivation and when does it occur?

Answer 224

When X-inactivation occurs in cells at a 90:10 ratio

1. Silencing of an abnormal X chromosome
2. Silencing of a normal X chromosome due to the other containing an abnormal autosomal translocation
3. (Random process 5-10% of the time)

Question 225

What is Turner syndrome?

What are 3 of the more common symptoms?

Answer 225

A genetic condition in which a female is partly or completely missing an X chromosome, leading to a plethora of possible symptoms that usually present in a unique way

1. Short stature
2. Webbed neck
3. Infertility

Question 226

What % of fetuses with Turner syndrome are born live?

How many females at birth are born with Turner’s? (1 in ?)

Answer 226

99% are spontaneously aborted while 1% are born alive.

1/2000 to 1/5000

Question 227

How does Turner syndrome arise? (3 ways)

What parent more often contributes the abnormal gamete?

Answer 227

1. The parent has a balanced translocation of the X chromosome and thus presents as asymptomatic
2. The mother has 45,X-mosacism affecting her maternal germ cells
3. Non-disjunction in the paternal cells, either at meiosis 1 or 2

Paternal cells more often contribute the abnormal gamete

Question 228

What causes the symptoms of Turner’s syndrome?

Answer 228

The presence of only one pseudoautosomal region

Question 229

List visible alterations seen in Turners syndrome (16)

Answer 229

1. Short stature
2. Lymphedema of hands and feet
3. Broad chest with widely spaced nipples
4. Low posterior hairline
5. Low-set ears
6. Increased weight / obesity
7. Shortened metacarpal (IV)
8. Hypoplastic or hyperconvex nails; small nails
9. Webbed neck
10. High waist to hip ratio
11. Microagnathia
12. Cubitus Valgus
13. Palmar crease
14. Drooping eyelids
15. Increased number of “birthmarks”
16. Madelung deformity of the wrist

Question 230

What are some physiological abnormalities seen in Turners Syndrome? (15)

Answer 230

1. Rudimentary ovaries/ gonadal streak –> infertility and amenorrhea
2. Aoertic valve stenosis
3. Coarctation of the aorta
4. Bicuspid aortic valve
5. Hypoplastic left heart syndrome
6. Partial anomalous venous drainage
7. Persistent hypertension
8. Aortic root dilation –> increased risk of aortic dissection/rupture
9. Horseshoe kidney
10. Abnormal urine collecting system
11. Visual impairments
12. Ear infections –> hearing loss
13. ADHD
14. Nonverbal learning disability (maths, social, spatial)
15. Red-green color blindness

Question 231

What are those with Turner’s syndrone at increased risk of? (think general) (6)

Answer 231

1. Kidney abnormalities
2. CV abnormalities
3. Bacterial endocarditis
4. Skeletal abnormalities
5. Diabetes
6. Hypothyroidism (often from Hashimoto’s hypothyroidism

Question 232

What are possible prenatal screening techniques for Tuner’s syndrome? (3)

Answer 232

1. Amniocentesis (with QFPCR)
2. Chorionic villus sampling (with FISH for X)
3. Abnormal U/S findings (heart defects, kidney abnormalities, cystic hygroma, ascites)

Question 233

What investigations can be done postnatally for Turner’s syndrome? (8/10)

Answer 233

1. Physical exam for the known symptoms
2. Karyotyping (choice of test)
3. Y-centromeric probe
4. LH/FSH (high <4 and >10; normal between 4-10)
5. TSH indicating hypothyroidism
6. Bone age (delayed after adolescence)
7. U/S for kidney/collecting system abnormalities
8. Echo or MRI for heart and aorta abnormalities

(9. Audiology testing for hearing loss)
(10. Urinalysis for DM)

Question 234

What can be done for the management of Turner’s syndrome?

Answer 234

1. GH +/- androgens starting at age 8 –> increase growth
2. Estrogen replacement at age 12-15 for bone strength, CV health, and pubertal changes
3. Thyroid hormones if necessary
4. Cosmetic surgery
5. Prophylactic antibiotics before any dental/surgical procedure
6. Reproductive technology
7. Calcium and vitamin D supplements
8. Antihypertensive agents
9. Physical activity and healthy diet

Question 235

What is premature ovarian failure / primary ovarian insufficiency? What are two major categories?

Answer 235

The loss of function of the ovaries before the age of 40.

1. Follicle depletion (low initial # or accelerated atresia)
2. Follicle dysfunction

Question 236

What is secondary ovarian insufficiency?

Answer 236

Loss of function of the ovaries before age 40 due to inadequate gonadotropin stimulation from inadequate LH/FSH production

Question 237

What are 10 causes of POF due follicualr depletion?

Answer 237

1. Disrupted germ cell formation
2. Thymic hypoplasia or aplasia inhibiting noral endowment of primordial follicles
3. X chromosome monosomy/aneuploidy (X0, XXX)
4. X chromosome mutations
5. Galactosemia
6. Cytotoxic therapy
7. Irradiation
8. Inflammation
9. Auto-immune conditions

Question 238

What are 9 causes of POF due follicualr dysfunction?

Answer 238

1. Idiopathic
2. Enzyme deficiencies (cholesterol desmolase, 17-alpha-OH)
3. FSH/LH receptor mutation
4. FSH receptor-blocking antibodies
5. Pseudohypoparathyroidism preventing cAMP production for signaling
6. Autoimmune oophoritis
7. Polyglandular autoimmune syndromes
8. Other immune disease (Hashimoto, DM type I, Vitiligo, Lupus, Sjögren, rheumatoid arthritis)
9. Infection

Question 239

What is the pathophysiology of POF?

Answer 239

1. Reduced/depleted follicle number or dysfunctional follicles leads to decreased production of progesterone, estrogen, and inhibin
2. This causes disinhibition of FSH and LH
3. As a result, normal follicular development will not occur
4. Overall estrogen further decreases and anovulation results
5. LH and FSH levels are increased by the HPOU axis to no avail.

Question 240

How do cysts form as a result of POF?

Answer 240

A lonely follicle may develop in the presence of high FSH, even though estrogen levels are low. However, the high LH will cause luteinization which may then persist as a cystic structure.

Question 241

How does POF present?

Answer 241

1. Missed or infrequent periods
2. Difficulty conceiving or complete infertility
3. Hot flashes and night sweats
4. Vaginal dryness with dyspareunia
5. CV disease
6. Osteoporosis

Question 242

What investigations are done in the work up for POF and its possible cause? What are possible results? (9)

Answer 242

1. Serum or urine beta-hCG for pregnancy
2. Serum FSH/LH levels –> both elevated, with FSH usually greater than LH (2x, 1 month apart)
3. Karyotype showing any X abnormalities
4. Genetic testing showing any known mutations associated
5. Antibody testing for adrenal or steroid cell antibodies
6. Ovarian U/S showing lack of follicles
7. Pituitary/hypothalamus MRI (rule out secondary ovarian failure)
8. DEXA for bone mineral density
9. Work up for other immune diseases (Adrenal antibodies, Antinuclear antigen antiboies, rheumatoid factors, thyroid peroxidase antibodies)

Question 243

What is the management plan for POF?

Answer 243

1. Hormone therapy with estrogen/progestin and possible androgen
2. In vitro fertilziation using a donor egg
3. Calcium, vitamin D supplementation
4. Weight-bearing exercise for 30 minutes per day, 3 days a week

Question 244

What is the difference between primary and secondary amenorrhea?

Answer 244

Primary amenorrhea = the absence of menarche

Secondary amenorrhea = amenorrhea for 3 consecutive cycles when a woman has had menstrual cycles in the past

Question 245

What are the 4 most common causes of secondary amenorrhea?

Answer 245

1. Pregnancy (implantation increases progesterone, preventing menstruation)
2. Hypothyroidism (increases AP activity and thus prolactin)
3. Prolactin disorders (prolactinemia, prolactinoma)
4. Medications (atypical antipsychotics)

Question 246

Fill in the following chart for how to investigate common causes of secondary amenorrhea.

Answer 246

Question 247

What are some possible causes of secondary amenorrhea? (16)

Answer 247

1. Pregnancy
2. Hypothyroidism
3. Prolactinoma / Prolactinemia
4. Atypical antipsychotics
5. Emotional stress
6. Anorexia and/or extreme exercise
7. AP adenoma
8. Sheehan’s Syndrome
9. Apoplexy of the AP
10. Savage (Resistant Ovarian Syndrome)
11. Menopause
12. POF/ POI
13. Autoimmune damage of the ovaries
14. Asherman’s syndrome
15. Ablation of the endometrius
16. PCOS

Question 248

How do you narrow down what is causing a secondary amenorrhea?

Answer 248

Question 249

Describe the progesterone challenge test:

Answer 249

1. Deliver progestin (Provera) 10 mg for 5 days (usually oral but can be IM)
2. After progestin, monitor for bleeding
3. If bleeding occurs between 2-7 days after progestin is stopped:
   - There is adequate estrogen in the body
   - There is functional anatomy
   - There is an anovulatory condition such as low progesterone or high androgen
4. If bleeding does not occur, give estrogen and progesterone together for 21 days
5. If bleeding occurs afterwards:

There is inadequate signaling –> a problem with the HPOU

6. If bleeding does not occur:
   - There is an endometrial problem

Question 250

Define oligomenorrhea

Answer 250

Infrequent or very light menstruation in a woman who once had regularly established periods

Periods occurring at intervals of greater than 35 days

Having 4-9 periods per year

Question 251

What is the female athlete triad?

Answer 251

A syndrome characterized by:

1. Eating disorder / energy deficiency
2. Amenorrhea / oligomenorrhea
3. Decreased BMD

Question 252

What can cause the female athlete triad?

Answer 252

1. Sports that emphasize low body weight
2. Vegetarian diets
3. Psychological predispositions
4. Social factors (family, self-esteem, abuse)
5. Genetics

Question 253

What are some symptoms of the female athlete triad? (9)

Answer 253

1. Disordered eating
2. Fatigue
3. Hair loss
4. Cold hands and feet
5. Dry skin
6. Noticeable weight loss
7. Increased healing time from injuries
8. Increased incidence of bone fracture
9. Amenorrhea / oligomenorrhea

Question 254

What are some possible findings in someone with female athelete triad? (9)

Answer 254

1. Elevated carotene in the blood
2. Anemia
3. Orthostatic hyotension
4. Irregular electrolytes
5. Low estrogen
6. Vaginal atrophy
7. Bradycardia
8. Mildly elevated cortisol
9. Low serum insulin and IGF-1

Question 255

What are possible things that can be done for someone with female athlete triad?

Answer 255

1. Diet change
2. Reduced exercise
3. Oral contraceptives
4. HRT
5. Mental health therapy
6. Calcium and vitamin D supplements
7. Bisphosphonates
8. Anti-depressents, benzodiazepines
9. Exogenous Kiss-peptin
10. Potassium supplements

Question 256

What is functional hypothalam amenorrhea (FHA)

Answer 256

Amenorrhea as a result of low energy availability, either as a result of decreased caloric intake, excessive energy use, increased stress, or a combination.

Question 257

What is nondisjunction in meisosis and what types of cells are created as a result?

Answer 257

Abnormal separation of chromosomes in meiosis I or sister chromatids in meiosis II

If it happens in meiosis I –> 2, 2, 0, 0 copies of genes

If it happen in meiosis II –> 1, 1, 2, 0 copies of genes

Question 258

What is monosomy? Give an example.

What is trisomy? Give 6 examples.

Answer 258

Monosomy = joining of a normal gamete with a gamete having no chromatids

• Ex. = Turner syndrome (X0)

Trisomy = joining of a normal gamete with a gamete having 2 chromatids

• Ex. = Down syndrome (21), Patau syndrome (13), Edwards syndrome (18), Klinefelter syndrome (XXY), Triple X syndrome (XXX) , XYY syndrome

Question 259

What is nondisjunction in mitosis and what types of cells are created as a result?

Answer 259

The abnormal separation of chromatids during anaphase

Creates one cell with 3 copies of affected genes and one cell with 1 copy of affected genes

Question 260

What is anaphase lag?

Answer 260

When something impairs movement of a chromatid during anaphse of mitosis, leading to its exclusion and loss from both daughters (one cell with 2 copies and one cell with 1 copy)

Question 261

What is endoreduplication?

Answer 261

When chromosomes duplicate but the cell does not divide, creating polyploid cells (binucleated) cells with 4 copies of chromosomes

Question 262

What is a hyrocele?

Answer 262

A pathological collection of serous fluid in the tunica vaginalis caused by injury and inflammation

Question 263

What is a variocele?

Answer 263

Swelling in the scrotum due to dilation of the veins that drain the testes

Question 264

What is infertility defined as?

Answer 264

The inability to reproduce by natural means after one year of unprotected intercourse

Question 265

What are the most common causes of female infertility? (6)

Answer 265

1. Ovulatory disorders
2. Endometriosis
3. Pelvic adhesions
4. Tubal blockage
5. Other tubal abnormalities
6. Hyperprolactinemia

Question 266

What are 3 ovarian causes of female infertility? (list sub-causes if possible)

Answer 266

1. Ovulatory disorders (pituitary damage, Kallman’s, hyperprolactinemia, stress)
2. Oocyte aging (smoking, radiation, chemo, autoimmune)
3. Ocarian cysts (endometriosis, PCOS)

Question 267

What are 6 fallopian tube/pelvic adhesion causes of female infertility? (list sub-causes if possible)

Answer 267

1. PID (chlamydia, gonorrhea)
2. Endometriosis
3. Adhesions from previous surgeries/infections (appendicitis, IBD)
4. Tb of fallopian tubes
5. Salpingitis isthmica nodosa = diverticulosis of fallopian tubes
6. Previous ectopic pregnancy

Question 268

What are 4 uterine causes of female infertility? (list sub-causes if possible)

Answer 268

1. Müllerian anomalies
2. Endometrial polyps
3. Intrauterine adhesions (D&C, C/S, myomectomy, Tb, idiopathic)
4. Deficient progesterone = luteal phase defect (pituitary problems)

Question 269

What are the 7 classes of Müllerian anommalies of the uterus?

Answer 269

1 = Uterine hypoplasia and/or agenesis

2 = unicornuate uterus

3 = uterus didelphys

4 = bicornuate uterus

5 = spetate uterus

6 = arcute uterus

7 = diethylstilbestrol (DES) drug related

Question 270

What are 2 cervical causes of female infertility? (list sub-causes if possible)

Answer 270

1. Congenital abnormalities
2. Trauma (accident, surgery, parturition)

Question 271

What are 6 causes of female infertility that are not due to the female reproductive tract

Answer 271

1. Turner syndrome
2. Antiphospholipid syndrome
3. Celiac disease (possibly)
4. BMI <19
5. Kidney failure
6. Liver failure

Question 272

What are 7 diagnostic tests for investigating the cause of female infertility?

Answer 272

1. Mucous stretch test = measure stretch of cervical mucous after sex

Hostile mucous will stretch <6cm, have no sperm, and/or have a negative Fern test

2. Ovulation work up

Anovulation indicated by no increase in basal temperature at day 14, no luteal progesterone elevation, and/or abnormal LH/FSH/estrogen

3. U/S to look for # of follicles, malformations, and endometrial lining
4. Measure Anti-mullerian hormone
5. Citrate test = inducing ovulation
6. Sonohistiogram to check patency, polyps, and fibroids
7. Laparascopic biopsy of endometrium to look for endometriosis

Question 273

What are some treatment options for female infertility? (7)

Answer 273

1. Administer clomiphrine citrate, which is an anti-estrogen, to trigger ovulation
2. Give estrogen/progesterone (OCP) to fix endometriosis if that’s the problem
3. Inject gonadotropins if deficient
4. Perform intrauterine insemination
5. Perform in vitro fertilization
6. Gestational donor
7. Surgery

Question 274

Define the following:

1. Oligozoospermia
2. Asthenozoospermia
3. Teratozoospermias
4. Azoospermia

Answer 274

1. Low number of sperm cells in the ejaculate (low [C])
2. Decreased sperm motility
3. Abnormal sperm morphology
4. Absence of sperm cells in the ejaculate

Question 275

What are the 4 categories of causes of male infertility

Answer 275

1. Idiopathic
2. Pre-testicular (endocrine and systemic)
3. Testicular
4. Post-testicular (sperm transport)

Question 276

What are 8 pre-testicular causes of male infertility? (list sub-causes if possible)

Answer 276

1. Hypogonadotropic hypogonadism (tumor, surgery, rads, chemo, trauma, vascular lesions, infiltrative disease, lymphocytic hypophysitis, Kallmann)
2. Hyperprolactinemia (prolactinoma, exogenous dopamine antagonist)
3. Panhypopituitarism
4. PAIS
5. CAH
6. Genetics affecting LH/FSH secretion (Prader-Willi, Lowe Oculocererbral, Familial cerebellar ataxia, Laurence-Moon-Biedl)
7. Drugs (estrogen, chronic glucocorticoids, opioids)
8. Obesity

Question 277

What are 13 testicular causes of male infertility? (list sub-causes if possible)

Answer 277

1. Idiopathic dysspermatogenesis
2. Tumors
3. PAIS
4. Cryptorchidism
5. Vanishing testes syndrome
6. Orchiditis (mumps, Tb, STDs, leprosy)
7. Varicoceles
8. Anti-sperm antibodies
9. Testicular damage (torsion, surgery, rads, chemo)
10. Testicular ischemia (CKD)
11. Genetic conditions (Klinefelter, Y chromosome mutations, DAZL polymorphisms, Myotonic dystrophy)
12. Drugs (antiandrogens, cyclophosphamide, estrogens)
13. Environment (smoking, hyperthermia, lead)

Question 278

What are 7 post-testicular causes of male infertility? (list sub-causes if possible)

Answer 278

1. Epididymis abnormalities (estrogen, obstruction, trauma)
2. Vas deferens abnormalities (gonorrhea, chlamydia, Tb, ligation, congenital absence)
3. Ejaculatory disorders (DM, neuropathy, spinal trauma)
4. Chronic infection of accessory glands
5. Cystic fibrosis
6. Primary ciliary dyskinesia
7. Sexual dysfunction (organic, psychogenic)

Question 279

Fill in the following chart for normal results of a semen analysis:

What are 4 variables looked at in semen microscopy?

Answer 279

1. Sperm (concentration, count, motility, morphology)
2. Debris/agglutination
3. Leukocyte count
4. Immature germ cells

Question 281

What investigations are done to determine the cause of male infertility? (6)

Answer 281

1. History (sexual development, sexual history, systemic illness, trauma, infections, surgery, drugs, environment)
2. Physical (thyroid signs, Cushing’s signs, external genitalia)
3. Semen analysis
4. Endocrine testing of LH/FSH/testosterone
5. Imaging of accessory glands/ducts
6. Genetic testing

Question 282

What are 5 possible treatments for male infertility?

Answer 282

1. Antibiotics (if caused by infection)
2. Hormone replacement therapy
3. Lifestyle changes (avoid long hot showers, wear loose underwear)
4. Artificial insemination (intrauterine insemination, in vitro fertilization, intro-cytoplasmic sperm injection)
   (5. Donor sperm)

Question 283

What is pelvic inflammatory disease?

Answer 283

An infection of the upper part of the female reproductive system (uterus, fallopian tubes, ovaries, inside pelvis)

Question 284

What causes PID?

Answer 284

Infectious organisms (usually anaerobic and facultative bacteria)

• Most commonly polymicrobial
• Most common bacteria are gonorrhea and chlamydia
• Other causative organisms are gardnerella, H. influenzae

Question 285

List some preventative causes of PID? (9)

Answer 285

1. Abstinence
2. Using condoms
3. Regular STI testing
4. Hormonal combined OCPs (thickens mucus plug)
5. Avoid vaginal activity after pregnancy until cervix closes
6. Reduce number of sexual partners
7. Take STI history from partners and encourage their testing
8. Avoid recreational drugs
9. Avoid vaginal douching

Question 286

What may help infectious organisms to descend from the vaginal os to the higher structures? (5)

Answer 286

1. Antibiotics affecting vaginal flora
2. Opened cervix during menstruation
3. Retrograde menstrual flow
4. Rhythmic uterine contractions during orgasm
5. Carried by sperm after intercourse

Question 287

What immune mechanism of the boyd is most implicated in PID?

Answer 287

Complement

Question 288

What are some symptoms of PID?

Answer 288

PID is often asynpmtomatic

1. Fever
2. Nausea/vomiting
3. Severe pelvic/abdominal pain (dull, achy, crampy, bilateral, constant, few days after menstruation, worse with movement, <7 days)
4. Abnormal vaginal discharge
5. Unanticipated vaginal bleeding (often after sex)

Question 289

What are 7 investigative procedures for PID? What results woudl you expect?

Answer 289

1. Physical exam (cervical motion/uterine/adnexal tenderness, peritonitis signs)
2. Lab studies (high WBC, ESR, bacteria, IgG, no UTI results, leukorrheal vaginal secretions)
3. Transvaginal U/S = thick/fluid filled tubes, thick cilia, indistinct endometrial borders, oophoritis, multiple ovarian cysts, free pelvic fluid, pelvic abscesses, ill-defined uterus)
4. Laparoscopy (tubal wall edema, visible hyperemia, exudate on tubal fimbriae)
5. MRI (hydrosalpinx, multiple ovarian cysts, ill-defined ovaries, thick-walled masses)
6. Culdocentesis (purulent fluid, leukocytes, bacteria)
7. Endometrial biopsy (possible scarring, organisms)

Question 290

What are 3 ways to diagnose PID?

Answer 290

1. Laparoscopically
2. Histopathologically
3. Clinically (sexually active + pelvic/abdo pain + cervical/uterine/adnexal tenderness + no other reason)

Question 291

What are complications of PID?

Answer 291

1. Scarring leading to chronic pain, infertility, ectopics, or infertility
2. Peritoneal inflammation causing scar tissue on external surface of liver

Question 292

What are the 2 treatment options for PID?

Answer 292

1. Antibiotics
   - Cefoxitin or cefotetan + doxycycline
   - Clindamycin + gentamicin
   - Ampicillin or sulbactam + doxycycline
2. Surgery if indicated
   - Simple drainage
   - Adhesiolysis
   - Copious irrigation
   - Unilateral adnexectomy

Question 293

What is ectopic pregnancy?

Answer 293

Implantation outside of the uterine cavity

• In the fallopian tube
• On the outside of the fallopian tube
• On the ovary
• On the abdominal wall
• On the outside of the bowel

Question 294

Ectopic pregnancy

1. What are 3 risk factors?
2. What is the presentation?
3. What investigations can you do?
4. How do you treat?

Answer 294

1. Tubal scarring, prior ectopics, IUDs
2. Unilateral pelvic or lower abdominal pain; vaginal bleeding
3. Speculum and bimanual, beta-hCG low for GA, U/S showing adnexal mass
4. Stabilize (fluid, blood, vasopressors); surgical laparotomy with possible salpingectomy or methotrexate if uncomplicated and small

Question 295

What are 3 causes of ectopic pregnancy?

Answer 295

1. Obstruction (ex. tumors, adhesions, sacrs, infections, clots)
2. Reduced endometrial responsiveness (ex. hormone dysregulation, infections, fibroids)
3. Embryonic defects

Question 296

What are 10 absolute contraindications to taking OCPs?

Answer 296

1. Thromboembolism
2. Pulmonary embolism
3. CAD
4. CV accident
5. Smoker over the age of 35
6. Breast/endometrial cancer
7. Unexplained vaginal bleeding
8. Abnormal liver function
9. Severe hypercholesterolemia
10. Severe hypertriglyceridemia

Question 297

What are 10 relative contraindications for OCPs?

Answer 297

1. Uterine fibroids
2. Lactation
3. DM
4. SCD
5. Hepatic disease
6. Hypertension
7. Lupus
8. Age 40+ with a high risk for vascular disease
9. Migraines
10. Seizure disorder

Question 298

What are 4 causes of abortion-induced death?

What is the rate of abortion-induced death?

Answer 298

1. Hemorrhage
2. Infection
3. Thromboembolism
4. Anesthetic complications

Rate = 1 in a million

Question 299

What is a threatened spontaneous abortion?

Answer 299

Any vaginal bleeding before 20 weeks without cervical dilation or fetus expulsion

Question 300

What causes spontaneous abortion in:

1. First trimester
2. Second trimester

Answer 300

First trimester:

• Mostly abnormal fetal chromosomes (usually a maternal gametogenesis error)
• Could be infection, immune problem, endocrine problem, maternal anatomic defect

Second trimester:

• Infection
• Maternal uterine/cervical defects (ex. incompetent cervix)
• Maternal systemic disease
• Fetotoxic agents
• Pre-term labour

Question 301

1. What is incompetent cervix?
2. Risk factors?
3. Presentation?
4. Treatment?

Answer 301

1. Dilation of the cervix causing exposure of fetal membranes to vaginal flora/trauma
2. Surgery, cervical trauma, congenital abnormality
3. Infection, discharge, rupture, dilation, short-term cramping/contraction, pressure in vagina, bleeding
4. Cerclage, tocolysis, bedrest

Question 302

Fill in the following chart:

Answer 302

Question 303

When a pre-natal screening test is positive, what are your options?

Answer 303

1. Paying for NIPS (non-invasive pre-natal screening)
2. Getting a detailed U/S for soft markers
3. Genetic counselling
4. Taking a diagnostic test (amniocentesis, CVS)

Question 304

What is pre-natal screening?

What are 4 methods?

Answer 304

Screening at 11+ weeks of pregnancy for common genetic anueploidies (trisomy 21, 18, and 13)

1. Maternal age
2. U/S (nuchal translucency, CR length, soft markers)
3. Maternal serum screen
4. Non-invaisve prenatal screening

Question 305

1. What is nuchal translucency?
2. What is a normal value?
3. What does an abnormal value indicate?
4. When is it performed?
5. What is its detection rate
6. What is its false positive rate?

Answer 305

1. Length of the sonolucent area in the nuchal region of the fetus on U/S
2. Normal = 3.0-3.5 or less
3. Increased risk of congenital anomalies (cardiac septa/abdominal wall/renal defects, diaphragmatic hernia) or malformation syndromes (NM disorder, skeletal dysplasia, Noonan, Smith-Lemli-Opitz)
4. week 11-13
5. 75-90%
6. 3-9%

Question 306

What are 6 maternal serum markers?

Answer 306

1. PAPP-A = pregnancy associated plasma protein A
2. Fee beta-hCG = hCG from placenta
3. PIGF = platelet growth factor
4. Alpha fetoprotein from baby’s liver (first and second TM types)
5. uE3 = unconjugated estriol from baby’s liver and placenta
6. DIA = dimeric inhibin-A from placenta

Question 307

Fill in the following chart with high or low:

Answer 307

Question 308

1. What is non-invasive prenatal screening?
2. What does it detect?
3. What is its detection rate?
4. What is its false positive rate?

Answer 308

1. Examining cell-free DNA in the mother’s blood
2. Increased DNA from the fetus may indicated trisomy 13/18/21/XXY/XYY
3. 99%
4. <1%

Question 309

What is multiple marker screening?

Give 4 examples.

Answer 309

Using multiple methods to create a reasonable risk assessment.

1. First trimester screening
2. Mid trimester screening
3. Integrated pre-natal screening
4. Enhanced first trimester screening

Question 310

Fill in the following chart regarding multiple marker screening examples.

Answer 310

Question 311

What are soft markers on U/S?

Which may indicate DS?

Answer 311

1. Nuchal translucency
2. Short femur
3. Echogenic intracardiac focus
4. Echogenic bowel
5. Short/absent nasal bone
6. Increased nuchal fold
7. Clinodactyly
8. Choroid plexus cysts
9. Dilated ventricles

DS = nuchal translucency, EICF (LR = 2), increased nuchal fold (LR = 17), echogenic bowel, short/absent nasal bone, clinodactyly

Question 312

What are 6 separate genetic errors that can result in trisomy 21 (Down Syndrome)?

Answer 312

1. Non-disjunction in early meiosis leading to a complete extra copy
2. Non-disjunction in early mitosis leading to a mosaic extra copy
3. Robetsonian translocations (new or balanced carrier parent)
4. Isochromosomes (1 arm duplicated, 1 arm lost)
5. Ring chromosomes
6. Spontaneous new mutation in the fetus

Question 313

What are 5 common and visible symptoms of Trisomy 21?

Answer 313

1. Transverse palmar flexure
2. Gap between first two toes
3. Flat facial profile
4. Epicanthal folds at eyes
5. Short stature (average man = 5ft 1in; average woman = 4ft; 8in)

Question 314

List 1 common defect in the following organs in those with Down Syndrome.

1. Heart
2. GI tract
3. Blood
4. Brain
5. Reproductive system

Answer 314

1. Atrial septal defects
2. Duodenal atresia
3. Acute lymphoblastic leukemia
4. Risk of Alzheimer’s Disease
5. Sterility (males)

Question 315

Fill in the following chart with different possible presentations of Down Syndrome

Answer 315

Question 316

What supports are available for management of Down Syndrome? (10)

Answer 316

1. Hearing aids
2. Tympanostomy tubes
3. CPAP machines
4. Therapy for speech and language
5. Occupational therapy
6. Education programs
7. Social/Family support
8. Medications for behavioural issues, mental illness, and RSV infetion prevention
9. Tonsillectomy
10. Plastic surgery

Question 317

What 9 things should those with Down Syndrome be screened for?

Answer 317

1. Hearing
2. Vision
3. T4/TSH levels
4. Teeth
5. Celiac disease
6. Sleep apnea
7. Neck X-ray
8. ECG/heart U/S
9. Testicles

Question 318

Fill in the following chart concerning appropriate pre-natal vitamin consumption to avoid pathology:

Answer 318

Question 319

What are 11 “normal” pathological changes in pregnancy?

Answer 319

1. Headaches
2. Edema
3. Nausea/vomiting
4. Heartburn
5. Constipation
6. Fatigue unrelieved by rest
7. Leg cramps
8. Round Ligament Pain
9. Varicose Veins
10. Hemorrhoids
11. Vaginal Discharge

Question 320

What is a teratogenic agent?

Answer 320

Any physical (drugs/rads), chemical, or infectious (microbial) agent that, on fetal exposure, can alter fetal morphology (and possibly function)

Question 321

What are 3 types of structural defects to a fetus?

Answer 321

1. Malformation = morpholgoic defect in an organ or body part due to abnormal first TM development
2. Deformation = abnormal form/shape/position of a body part due to constraint
3. Disruption = defects from interference with a normally developing organ system (after organogenesis usually)

Question 322

What are the 3 stages of fetal development in regards to teratogenic susceptibility?

Answer 322

1. Resistant (all or nothing) = day 0-11
2. Maximum susceptibility = day 11-57 (organogenesis)
3. Lowered susceptibility = day 57 onward (histogenesis)

Question 323

What 4 important organs/systems are still susceptible to teratogens after organogenesis (week 9 onward)

Answer 323

1. Fetal eyes
2. Genitalia
3. Hematopoietic system
4. CNS

Question 324

What are the 6 main categories of teratogens?

Answer 324

1. Radiation
2. Drugs/medications
3. Hyperthermia
4. Hyperglycemia
5. Phenylketonuria
6. Infection

Question 325

Radiation as a teratogen:

1. What doses are ok?
2. What are sources?
3. What are the effects from week 2-4? 4-12? 12-16? 20+?

Answer 325

1. 5-10
2. Imaging diagnostics, radiation therapy

Week 2-4 = abortion;

Week 4-12 = microcephaly, retardation, cataracts, small eyes

Week 12-16 = retardation

Week 20+ = hair loss, skin lesion, bone marrow suppression

Question 326

What drug factors determine whether it will have an effect on the fetus? (6)

Answer 326

1. Maternal absorption
2. Metabolism
3. Protein binding/storage
4. Molecular size (>1,000 Da don’t easily cross placenta)
5. Electrical charge
6. Lipid solubility

Question 327

List 10 common drug teratogens and their common effects

Answer 327

1. Alcohol - FAS
2. Heroin - neonatal withdrawal
3. Phencyclidine - facial abnormalities
4. Cocaine - congenital abnormalities, stillbirth, LBW
5. Chemotherapy - IUGR, stillbrith, LBW, preterm
6. Anti-epileptics (valproic acid, phenytoin, carbamazepine) - NTD
7. Lithium - Ebstein’s anomaly
8. SSRIs - cardiac septal defects, persistent hypertension
9. Benzodiazepines - cleft anomalies
10. Warfarin - fetal warfarin syndrome
11. ACEI - renal duysfunction, IGUR, oligohydramnios
12. Vitamin A derivates (isoretinoin, accutane) - CNS/thymus problems, limb reduction, developmental delay, microagnathia

Question 329

What are 10 features of the fetal warfarin syndrome?

Answer 329

1. Flattened nasal bridge
2. Stippled bony epiphyses
3. Occular defects
4. Extremity hypoplasia
5. Developmental retardation
6. Seizures
7. Scoliosis
8. Deafness/hearing loss
9. Congenital heart disease
10. IGUR

(possible death)

Question 330

What are 9 features of fetal alcohol syndrome?

Answer 330

1. Small head
2. Epicanthal folds
3. Flat midface
4. Smooth philtrum
5. Low nasal bridge
6. Small eye openings
7. Short nose
8. Thin upper lip
9. Underdeveloped jaw

Question 331

What 13 infections can be teratogenic? (CHEAPTORCHES)

Answer 331

1. Chickenpox/shingles (varicella zoster virus)
2. Hepatitis B, C, D, E
3. Enteroviruses
4. AIDS
5. Parovirus B19
6. Toxoplasmosis
7. Group B Streptococcus
8. Listeria
9. Candida
10. Rubella
11. Cytomegalovirus
12. Herpes simplex virus
13. Syphilis

Question 332

Rubella virus:

1. When does the virus have the most effects?
2. What happens in congenital rubella syndrome? (13)

Answer 332

1. First month affects 90%, second month affects 22%
2. Microcephaly, mental/motor retardation, meningoencephalitis, persistent patent DA, pulmonary artery stenosis, AV septal defects, cataracts, microphthalmia, retinal changes, blindness, sensorineural deafness, IUGR

Question 333

Varicella Zoster Virus:

1. When does the virus have the most effects?
2. What happens in congenital varicella? (13)

Answer 333

1. First TM affects 2% but severely; Second TM affects 25% but less severely; no effect 28-40 weeks
2. Skin scarring/rash, limb hypoplasia, clubfoot, microcephaly, seizures, retardation, autonomic dysfunction, microphthalmia, cataracts, IUGR, fever, pneumonia, death

Question 334

What are pre-existing risk factors for thromboembolic disease in pregnancy? (4)

Answer 334

1. Obesity
2. Advanced maternal age
3. Previous clots
4. Thrombophilic disorders

Question 335

What are complicated outcomes of thromboembolic disease in pregnancy? (6)

Answer 335

1. DVT
2. PE
3. Hypertensive disorder
4. Pre-eclampsia
5. SGA infant
6. Future recurrent miscarriages

Question 336

What are treatment options for thromboembolic disease in pregnancy?

Answer 336

1. Unfractionated heparin
2. Low-molecular-weight heparin (up until week 35)
3. Aspiring (up until week 16)
4. Warfarin (after pregnancy)

Question 337

What is antiphospholipid antibody syndrome?

Answer 337

An autoimmune hypercoagulable state caused by antiphospholipid antibodies

Question 338

What is Asherson syndrome?

Answer 338

APLS leading to rapid organ failure and generalised thrombosis

Question 339

What 3 proteins are targeted by self-antibodies in APLS?

What are these antibodies?

Answer 339

1. Beta-2 glycoproteins –> Lupus anticoagulant antibody
2. Annexin 2-5 –> Anti-annexin antibody
3. ApoH / cardiolipin –> Anticardiolipin antibody

Question 340

What are 3 reasons for hypercoagulability in APLS?

Answer 340

1. Inhibition of protein C by anti-cardiolipin antibodies binding ApoH
2. Inhibition of protein S further decreasing protein C activity
3. Inhibition of prothrombin by lupus anticoagulant

Question 341

What are pregnany related risks of APLS? (6)

Answer 341

1. Miscarriage
2. Stillbrith
3. Pre-term devliery
4. Severe pre-eclampsia
5. IUGR
6. Mental/developmental retardation

Question 342

What are 4 diagnostic tecniques used in the workup of APLS?

Answer 342

1. Prolonged PTT, not correcting on addition of normal plasma
2. Liquid phase coagulation assays to check for lupus anticoagulant antibodies
3. Solid phase ELISA assay to check for anticardiolipin antibodies
4. Genetic screen for underlying thrombophilia

Question 343

What is required for a clinical diagnosis of APLS? (2)

Answer 343

1. Documented episode of arterila/venous/small vessel thrombosis in a deep vein in the absence of inflammation
2. 1+ fetal deaths at >10 weeks and/or 3+ fetal deaths at <10 weeks

Question 344

What are 3 possible ways to diagnose APLS based on lab values?

Answer 344

1. Anti-cardiolipin IgG and/or IgM on 2+ occassions less than 8 weeks apart
2. Anti-beta2 glycoprotein IgG and/or IgM on 2+ occassions less than 8 weeks apart
3. Lupus anticoagulant detected on 2_ occassions less than 8 weeks apart

Question 345

What are treatment options for APLS?

Answer 345

1. Aspirin
2. Warfarin (after pregnancy)
3. Heparin (during pregnancy)

Question 346

Postterm Pregnancy

1. Define
2. List 5 causes
3. How is it managed?

Answer 346

1. Pregnancy extended beyond 42 weeks’ gestation
2. Wrong LMP, anencephaly, congenital primary fetal adrenal hypoplasia, placental sulfatase deficiency, idiopathic
3. Expectant until delivery is indicated via the biophysical profile, labour induction when indicated

Question 347

Biophysical profile

1. What factors does it assess?
2. Fill out the chart:

Answer 347

1. Non-stress test, fetal breathing, fetal tone, fetal motion, quantity of amniotic fluid

Question 348

What is the diagnostic criteria for each stage of labour to be considered “prolonged” in nulli vs. multiparous women?

How do you manage it in each stage?

Answer 348

Stage 1 latent = >20 hours (N) or >14 hours (M)

• Treat with balloon catheter, amniotomy, oxytocin

Stage 1 active = no change in 4 hours or 5 hours total (N and M)

• Treat with oxytocin and if this fails do a C/S

Stage 2 = >2 hours (N) or >1 hour (M)

• Treat with oxytocin and if this fails do a C/S (negative cm) or forceps/vacuum (positive cm)

Stage 3 = >30 minutes (N and M)

• Uterine massage –> oxytocin –> manual extraction –> D&C surgery

Question 349

Define placenta accreta, placenta increta, and placenta percreta.

Answer 349

Placenta accreta = chorionic villi attach to myometrium

Placenta increta = chorionic villi invade the myometrium

Placenta percreta = chorionic villi invade the perimetrium (serosa)

Question 350

Define:

1. Pre-term ROM
2. Premature ROM
3. Pre-term premature ROM
4. Prolonged ROM

Answer 350

1. ROM before week 37
2. ROM during week 37-45 but more than 1 hour before onset of labour
3. premature ROM during week 24-37
4. Normal ROM, but followed by 18 hours with no labour

Question 351

Abnormal ROM:

1. What are 4 ways to confirm ROM has taken place?
2. What is a common cause of abnormal ROM?
3. How are abnormal ROM treated? (PPROM, PROM, prolonged)
4. What are 2 complications of prolonged ROM?

Answer 351

1. Pooling of fluid seen in vagina, nitrazine test (blue), positive fern test, U/S showing olighydramnios
2. Group B Strep Infection
3. PPROM = deliver if <24 or >34; steroids if 24-34

PROM = induce delivery +/- ampicillin

Prolonged ROM = induce delivery +/- ampicillin

4. Chorioamnionitis before delivery; endometritis after delivery

Question 352

Define:

1. Complete placental previa
2. Partial placental previa
3. Marginal placental previa

Answer 352

1. Placenta completely covering cervical os
2. Placenta partially covering cervical os
3. Placenta ending within 2 cm of cervical os

Question 353

Placenta previa

1. What are 4 risk factors
2. What is the presentation?
3. What are 3 complications?
4. What are 4 possible management steps?

Answer 353

1. Twins/triplets, maternal age >35, intrauterine fibroids, maternal smoking
2. Intermittent or continuous bleeding after 20 weeks gestation
3. Maternal loss of blood, fetal hypoxia, pre-term delivery
4. Corticosteroids, bed rest, blood products/IV fluids, C/S

Question 354

Breech presentation:

1. Define
2. What are 2 (categories of) causes?
3. What are 2 complications?
4. How is treated? (2)

Answer 354

1. Fetus exiting the birthing canal bottom first and head last
2. Inability of fetus to move; insufficient intrauterine space for movement
3. Oxygen deprivation; brain/skull injury
4. External cephalic version +/- tocolytics, C/S

Question 355

Cephalopelvic disproportion:

1. Define
2. List some causes
3. How is treated?

Answer 355

1. Baby’s head is too large in relation to maternal pelvis, either form large head or small/abnormal shaped pelvis
2. Hereditary macrosoma, diabetes, post-term baby, maternal vitamin D deficiency, young maternal age, materanl obstructive tumor

Question 356

Shoulder dystocia:

1. Define
2. What are 5 risk factors?
3. What are 3 signs?
4. What is the treatment?

Answer 356

1. Obstructed labour after the delivery of the head due to the anterior shoulder not being able to pass through the pelvis
2. Maternal age >35, short mother, small/abnormal maternal pelvis, post-term labour, maternal diabetes
3. Turtle sign, erythematous puffy fetal face, failure to deliver shoulders after head
4. Leg hyperfelxion, applying pressure, episiotomy, mother getting on all fours, break the baby’s clavicle

Question 357

Intrauterine hypoxia:

1. Define
2. What are 4 causes?
3. What are 2 complications?
4. What is 1 treatment option?

Answer 357

1. Deprivation of adequate oxygen to the fetus
2. Prolapse/occlusion of umbilical cord, placental infarction, maternal smoking, IUGR
3. CNS damage, fetal acidosis
4. Hypothermia therapy = lowering baby’s core body temperature

Question 358

What is the difference between induction and augmentation of labour?

Answer 358

Induction = initiating labour before any spontaneous onset, with the goal of vaginal delivery

Augmentation = enhancing uterine contractiliy when labour has already begun

Question 359

What is the Bishop score?

What are its components?

What do scores mean?

Answer 359

A cervical scoring system used to determine the potential success of labour induction.

Uses 5 criteria:

1. Cervical dilation (cm)
2. Cervical effacement (%age)
3. Cervical consistency
4. Cervical position
5. Fetal station

6+ = high likelihood of successful labour

<6 = reduced likelihood of successful labour –> induce cervical ripening

Question 360

How are values determined in the Bishop score?

Answer 360

Question 361

What are the absolute indications for inducing labour?

(4 maternal; 4 fetal)

Answer 361

Maternal = pre-eclampsia, DM/CKD/CPD complications

Fetal = chorioamnionitis, post-term, IUGR, isoimmunisation

Question 362

What are the relative indications for inducing labour?

(4 maternal; 4 fetal; 1 uteroplacental)

Answer 362

Maternal = chronic/gestational HT, gestational DM, history of rapid labour, far from a hospital

Fetal = Premature ROM, macrosomia, demise, major anomaly

Uteroplacental = unexplained oligohydramnios

Question 363

What are the absolute contra-indications for inducing labour?

(2 maternal; 3 fetal; 4 uteroplacental)

Answer 363

Maternal = active genital herpes, serious chronic medical condition

Fetal = mal-presentation, no fetal head flexion, fetal distress

Uteroplacental = cord prolapse, placenta previa, vasa previa, prior C/S

Question 364

What are the relative contra-indications for inducing labour?

(2 maternal; 1 fetal; 4 uteroplacental)

Answer 364

Maternal = cervical carcinoma, pelvic deformities

Fetal = extremely large

Uteroplacental = low-lying placenta, unexplained vaginal bleeding, cord presentation, myomectomy

Question 365

What are 4 ways to ripen a cervix?

Answer 365

1. Hormones (prostaglandins, oxytocin, estrogen, mifepristone, relaxin)
2. Amniotomy
3. Membrane stripping
4. Mechanical dilation (hygroscopic dilation, balloon catheter)

Question 366

What are 2 ways to induce labour?

Answer 366

1. Hormones (oxytocin, prostaglandin, mifepristone)
2. Amniotomy

Question 367

What are 3 risks involved in inducing labour?

Answer 367

1. Hypoxia –> oxytocin and prostaglandin may cause abnormal/excessive contractions which diminish baby’s oxygen supply
2. Infection from ROM
3. Post-partum hemorrhage –> induction may increase uterine muscle exhaustion or exogenous hormones may prevent uterine contraction around spiral arteries

Question 368

What do the following indicate:

1. Type I deceleration of FHR
2. Type II/delayed deceleration of FHR
3. Variable FHR

Answer 368

1. Nothing to worry about
2. Hypoxia
3. Compression of umbilical cord