Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > Basic Anatomy Review > Flashcards

Basic Anatomy Review Flashcards

1
Q

Hypothalamus releases

A 
Corticotropin RH
Gonadotropin RH 
Thyrotropin RH 
Growth hormone RH 
Antidiuretic hormone 
Oxytocin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Thyroid gland releases

A

Triiodothyronine (T3)

Thyroxine (T4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adrenal gland releases

A

Cortex -
aldosterone
cortisol
androgens

Medulla -
catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Testes release

A

testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pituitary gland releases

A 
Anterior - 
Growth hormone 
Prolactin 
Luteinizing hormone 
Follicle-stimulating hormone 
Thyroid stimulating hormone 
Adrenocorticotropic hormone

Posterior pituitary -
Antidiuretic hormone
Oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are ADH and oxytocin produced

A

ADH and oxytocin are produced in the hypothalamus and stored in the posterior pituitary gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Parathyroid glands release

A

Parathyroid hormone (PTH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pancreas releases

A

insulin

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ovaries release

A

estrogen

progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hypothalamic pituitary axis role

A

Information about cortical inputs, automatic function, environmental cues (light, temperature) and peripheral hormonal feedback is synthesized at the coordinating centre of the endocrine system, the hypothalamus.

The hypothalamus then sends signals to the pituitary to release hormones that affect the thyroid, adrenals, gonads, growth, milk production, and water balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adrenal gland composition and function

A

Each gland (6-8 g) has

1) a cortex with 3 layers that act like independent organs
(zona glomerulosa -> aldosterone,
fasciculata -> cortisol,
reticularis -> androgen and estrogen precursors), and

2) a medulla that acts like a sympathetic ganglion to store/synthesize adrenaline and noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Function of gonads

A

Bifunctional: sex steroid synthesis and gamete production

Sex steroids control sexuality and affect metabolic and brain functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chylomicron function

A

Transports dietary TG from gut to adipose tissue and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

VLDL function

A

Transports hepatic synthesized TG from liver to adipose tissue and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IDL function

A

Product of hydrolysis of TG in VLDL by lipoprotein lipase resulting in depletion of TG core

Enriched in cholesterol esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

LDL function

A

Formed by further removal of residual TG from IDL core by hepatic lipase resulting in greater enriched particles with cholesterol esters

Transports cholesterol from liver to peripheral tissues (gonads, adrenals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

HDL function

A

Transports cholesterol from peripheral tissues to liver Acts as a reservoir for apolipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Exogenous and endogenous biosynthetic lipid pathways

A

TN E3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Familial lipoprotein lipase deficiency etiology/pathophysiology

A

Autosomal recessive deficiency of lipoprotein lipase or its cofactor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Familial lipoprotein lipase deficiency labs

A

Increased TG

Increased chylomicrons

Moderate increase in VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Familial lipoprotein lipase deficiency clinical presentation

A 
Presents at infancy 
Recurrent abdominal pain 
Hepatosplenomegaly 
Splenic infarct 
Anemia, granulocytopenia, thrombocytopenia 2o to hypersplenism 
Pancreatitis 
Lipemia retinalis 
Eruptive xanthomata
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Familial lipoprotein lipase deficiency treatment

A

Decrease dietary fat intake to <10% of total calories

Decrease dietary simple carbohydrates

Cook with medium chain fatty acids

Abstain from EtOH

Gene therapy (Glybera)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Familial hypertriglyceridemia etiology/pathophysiology

A

Autosomal dominant for inactivating mutations of the LP lipase gene Several genetic defects resulting in increased hepatic VLDL synthesis or decreased removal of VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Familial hypertriglyceridemia labs

A

Increased TG

Increased VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Familial hypertriglyceridemia clinical presentation

A

Possible premature CAD

Develop syndrome of obesity, hypertriglyceridemia, hyperinsulinemia, and hyperuricemia in early adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Familial hypertriglyceridemia treatment

A

Decrease dietary simple carbohydrates and fat intake

Abstain from EtOH

Fibrates or niacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Types of primary hypertriglyceridemias

A

Familial lipoprotein lipase deficiency

Familial hypertriglyeridemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Secondary hypertriglyceridemia etiologies

A
  • endocrine: obesity/metabolic syndrome, hypothyroidism (more for high LDL, not TG), acromegaly, Cushing’s syndrome, DM
  • renal: chronic renal failure, polyclonal and monoclonal hypergammaglobulinemia
  • hepatic: chronic liver disease, hepatitis, glycogen storage disease
  • drugs: alcohol, corticosteroids, estrogen, hydrochlorothiazide, retinoic acid, β-blockers without intrinsic sympathomimetic action (ISA), anti-retroviral drugs, atypical antipsychotics, oral contraceptive pills
  • other: pregnancy
29
Q

Hypertriglyceridemia and pancreatitis

A

Serum triglyceride levels >10 mmol/L increases the risk of developing pancreatitis (even some reports of TG >5 mmol/L)

30
Q

Types of primary hypercholesterolemias

A

Familial hypercholeseterolemia

Polygenic hypercholesterolemia

Familial combined hyperlipidemia

31
Q

Familial hypercholesterolemia etiology/pathophysiology

A

Most commonly due to defects in the normal LDL receptor on cell membranes

1/500 in U.S. population Autosomal codominant with high penetrance More prevalent in French Canadian, Dutch Afrikanner, Christian Lebanese populations

32
Q

Familial hypercholesterolemia clinical presentation

A

Tendinous xanthomatosis (Achilles, patellar, and extensor tendons of hand)

Arcus cornealis

Xanthelasmata

Heterozygotes: premature CAD, 50% risk of MI in men by age 30

Homozygotes: manifest CAD and other vascular disease early in childhood and can be fatal (in <20 yr olds)

33
Q

Familial hypercholesterolemia treatment

A

Heterozygotes: improvement of LDL with statins, often in combination with ezetimibe or bile acid sequestrants or PCSK9 inhibitor

Homozygotes: partial control with portacaval shunt or LDL apheresis in conjunction with niacin; large dose statin is modestly effective; potential liver transplant; consider lomitapide (inhibitor of the microsomal TG transfer protein) and mipomersen (inhibits ApoB gene)

34
Q

Familial hypercholesterolemia labs

A

Inc LDL

Inc TC

35
Q

Familial hypercholesterolemia and cardiovascular risk calculators

A
  • Risk calculators such as Framingham and SCORE do not apply to patients with familial hypercholesterolemia
  • Consider all adults with FH as “high risk”
36
Q

Polygenic Hypercholesterolemia etiology/pathophysiology

A

Most common

Few mild inherited defects in cholesterol metabolism

37
Q

Polygenic Hypercholesterolemia labs

A

Inc TC

Inc LDL

38
Q

Polygenic Hypercholesterolemia clinical presentation

A

Asymptomatic until vascular disease develops

No xanthomata

39
Q

Polygenic Hypercholesterolemia treatment

A

Statins, ezetimibe, niacin, bile acid sequesterant, PCSK9 inhibitor

40
Q

Familial Combined Hyperlipidemi etiology/pathophysiology

A

In many cases, over-population of VLDL and associated inc LDL 2o to excess hepatic synthesis of apolipoprotein B

Autosomal dominant

  • A common disorder (1-2% of the population)
  • Contributes to 1/3 to 1/2 of familial coronary artery disease
41
Q

Familial Combined Hyperlipidemi labs

A

inc TC + G
inc VLDL
inc LDL

42
Q

Familial Combined Hyperlipidemi clinical presentation

A

Xanthelasma

CAD and other vascular disease

43
Q

Familial Combined Hyperlipidemi treatment

A

Weight reduction

Decrease simple carbohydrates, fat, cholesterol, and EtOH in diet

Statins Niacin, fibrates, ezetimibe, PCSK9 inhibitor

44
Q

Secondary hypercholesterolemia etiologies

A
  • endocrine: hypothyroidism
  • renal: nephrotic syndrome
  • immunologic: monoclonal gammopathy
  • hepatic: cholestatic liver disease (e.g. primary biliary cirrhosis)
  • nutritional: diet, anorexia nervosa
  • drugs: cyclosporin, anabolic steroids, carbamazepine
45
Q

Familial hypoalphalipoproteinemia or Familial HDL deficiency etiology/pathophysiology

A

Autosomal dominant inheritance of a mutation in the ABCA1 or the APOA1 gene

46
Q

Familial hypoalphalipoproteinemia or Familial HDL deficiency clinical presentation

A

Premature atherosclerosis

Cerebrovascular disease

Premature atherosclerosis

Xanthomas

47
Q

Familial hypoalphalipoproteinemia or Familial HDL deficiency treatment

A

Reduce the risk of atherosclerosis with lifestyle changes, management of concomitant hypercholesterol-emia, hypertriglyceridemia, and metabolic syndrome if present

48
Q

Tangier disease etiology/pathophysiology

A

Autosomal recessive inheritance of mutations in the ABCA1 gene

Impaired HDL-mediated cholesterol efflux from macrophages and impaired intracellular lipid trafficking

49
Q

Tangier disease clinical presentation

A

Mild hypertriglyceridemia

Neuropathy

Enlarged, orange-coloured tonsils

Premature atherosclerosis

Splenomegaly Hepatomegaly

Corneal clouding

Type 2 DM

50
Q

Tangier disease treatment

A

Reduce the risk of atherosclerosis with lifestyle changes, management of concomitant hypercholesterol-emia, hypertriglyceridemia, and metabolic syndrome if present

51
Q

Low HDL secondary causes

A
  • endocrine: obesity/metabolic syndrome, DM
  • drugs β-blockers, benzodiazepines, anabolic steroids
  • other acute infections, inflammatory conditions
52
Q

Treatment effect of LDL reduction

A

Each 1.0 mmol/L decrease in LDL corresponds to 20-25% relative risk reduction in cardiovascular disease

53
Q

Dyslipidemia and the risk for coronary artery disease

A
  • increased LDL is a major risk factor for atherosclerosis and CAD as LDL is the major atherogenic lipid particle
  • increased HDL is associated with decreased cardiovascular disease and mortality
  • moderate hypertriglyceridemia (triglyceride level 2.3-9 mmol/L) is an independent risk factor for CAD, especially in people with DM and in post-menopausal women
  • treatment of hypertriglyceridemia has not been shown to reduce CAD risk
54
Q

What is the 6% rule

A

if dose of statin is doubled there is ~6% inccrease in the LDL lowering efficacy

55
Q

When to screen for dyslipidemia

A

• screen men >40 yr, women >50 yr or post-menopausal

• if following risk factors present, screen at any age:
■ DM
■ current cigarette smoking or COPD
■ HTN (sBP >140, dBP >90)
■ obesity (BMI >27 kg/m2)
■ family history of premature CAD
■ clinical signs of hyperlipidemia (xanthelasma, xanthoma, arcus cornealis)
■ evidence of atherosclerosis
■ inflammatory disease (rheumatoid arthritis, SLE, psoriatic arthritis, ankylosing spondylitis, inflammatory bowel disease)
■ HIV infection on highly active anti-retroviral therapy (HAART)
■ chronic kidney disease (estimated GFR <60 mL/min/1.73 m2)
■ erectile dysfunction

screen children with a family history of hypercholesteerolemia or chylomicronemia

56
Q

for statin follow-up

A
  • Liver enzymes and lipid profile: liver enzymes measured at the beginning of treatment then once after therapy initiated. Lipids (once stabilized) measured annually. Order both if patient complains of jaundice, RUQ pain, dark urine
  • CK at baseline and if patient complains of myalgia
  • D/C statin if CK >10x upper limit of normal or patient has persistent myalgia
57
Q

Factors affecting dyslipidemia risk assessment

A

• metabolic syndrome

• apolipoprotein B (apo B)
■ each atherogenic particle (VLDL, IDL, LDL, and lipoprotein A) contains one molecule of apo B
■ serum [apo B] reflects the total number of particles and may be useful in assessing cardiovascular risk and adequacy of treatment in high risk patients and those with metabolic syndrome

• C-reactive protein (hs-CRP) levels
■ highly sensitive acute phase reactant
■ may be clinically useful in identifying those at a higher risk of cardiovascular disease than predicted by the global risk assessment

58
Q

Dyslipidemia practice guidelines

A

ACC/ AHA is no longer recommending a Treat to Target” approach for statin theapy Primary prevention in patients with increased risk should be treated with moderate to high intensity statin therapy without tracking LDL targets. Similarly, patients needing secondary prevention should receive high intensity statn therapy without attention to LDL targets

59
Q

Primary prevention for dyslipidemia

A

■ estimate 10 yr risk of CAD using Framingham Risk Score (FRS) model

■ establish treatment targets

■ low FRS does not require statin treatment

60
Q

Statin indicated conditions

A

Clinical atherosclerosis

Abdominal aortic aneurysm

DM >15 yr duration and age older than 30 yr

DM with age older than 40 yr

DM with microvascular disease

Chronic kidney disease and age older than 50yr

LDL-C≥ 5mmol/

61
Q

Statin indicated conditions primary target LDL-C

A

≤2 mmol/L
or ≥50% decrease in LDL

For LDL-C ≥5mmol/L: 50% decrease in LD

62
Q

Statin indicated conditions alternate target

A

apo B ≤0.80 g/L

or non-HDL-C
≤2.6 mmol/L

63
Q

What is considered high and intermediate risk FRS

A

High risk FRS 20%+

Intermediate risk FRS 10-19%

64
Q

When to initiate treatment of dyslipidemia with statins outside of statin indicated conditions

A

high or intermediate risk FRS

LDL >3.5 mmol/L

For LDL-C<3.5 consider if: apo B ≥1.2 g/L or non-HDL-C ≥4.3 mmol/L

65
Q

dyslipidemia outside of statin indicated conditions primary target LDL-C

A

≤2 mmol/L

or ≥50% decrease in LDL

66
Q

dyslipidemia outside of statin indicated conditions alternate target

A

apo B ≤0.80 g/L

or non-HDL-C ≤2.6 mmol/

67
Q

Treatment of hypercholesterolemia

A

Conservatve:
4-6 mo trial unless high risk group, in which case medical treatment should start immediately

Diet: Decrease fat: <30% calories 
Decrease saturated fat: <10% calories 
Decrease cholesterol: <200 mg/d 
Increase fibre: >30 g/d 
Decrease alcohol intake to ≤1-2 drinks/d 
Smoking cessation 
Aerobic exercise: ≥150 min/wk in bouts of ≥10 min 
Weight loss: target BMI <25

Medical: HMG-CoA reductase inhibitors, ezetimibe, bile acid sequestrants, niacin

68
Q

Treatment of hypertriglyceridemia

A

Conservative: 4-6 mo trial Diet: Decrease fat and simple carbohydrates Increase omega-3 polyunsaturated fatty acid Control blood sugars Decrease alcohol intake to ≤1-2 drinks/d Smoking cessation Aerobic exercise: ≥150 min/wk in bouts of ≥10 min Weight loss: target BMI <25

Medical: fibrates, niacin

Indications for medical: Failed conservative measures
TG >10 mmol/L (885 mg/dL) to prevent pancreatitis
Combined hyperlipidemia

69
Q

Rosuvastatin to prevent vascular events in men and women with elevated CRP

A

Statins reduce the incidence of major cardiovascular events even in healthy people without hyperlipidemia but with elevated creactive protein.

Endocrinology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions