Brainscape's Knowledge GenomeTM

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


See full index

BPT > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Which MODY uses sulfonylurea for treatment?

A

MODY3

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

Diagnostic criteria for diabetes

A

Hba1c > 6.5%
Fasting glucose > 7
Random glucose > 1.1
OGTT - meeting above criteria

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

GDM diagnosis

A

OGTT 24-28 weeks
Fasting > 5
1 hour > 10
2 hour > 8.5

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

MoA of metformin

A

Suppresses hepatic gluconeogenesis

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

SLGT2 benefit in diabetic nephropathy - mechanism

A

Reduce intraglomerular pressure due to increased afferent arteriole resistance

Reduced hyperfiltration

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

Which SGLT2 has higher risk of amputations?

A

Canglifozin

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

Benefit of degludec vs lantus/levemir

A

Reduces overnight hypoglycaemia

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

Types of Type 1 Diabetes

A

Type 1A - immune.
- Usually polygenetic
- Monogenic - AIRE (Polyendocrinopathy), FOXP3 (IPEX)

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

Polyendocrinopathy
X linked
Enteropathy

A

IPEX

FOXP3 gene

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

HLA associated with diabetes

A

HLA DR3 and HLA DR4 (have both = 50%)

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

Pathophys of T1DM

A

T cell mediate process

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

T1DM Ab’s

A

GAD
Insulin
IA-2
ZnT8

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

Anti-CD3 reducing time of onset T1DM

A

Tepiluzimab

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

Name of principal where long term complications of diabetes occur if there is poor control early

A

Metabolic memory

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

Glargin vs detemir

A

Gargine - hexamers under skin, delay absoprtion

Detemir - binds albumin, prolongs half life

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

Meal ratio calculation

A

500/TDD

1 unit of insulin for how many g for of CHO

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

Insulin sensitivity factor

A

100/TDD

1 unit of insulin drops BGL by how manny mmol/L

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

Evidence for CGM (continuous gucose monitor)

A

REduction in Hba1c
Reduces hypos
Improves time in range (closed loop therapy)

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

Whipple’s triad

A

Symptoms of low BGL
Low BGL
Symptoms imrpove after correcting BGL

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

Lymphocytic hypophysitis
- Features
- Differentiate from Sheehan syndrome

A

Hypopituitarism and headaache postpartum, no PPH

Sheehan - PPH, ischaemic infarction of pituitary causing hypopituitarism

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

Apoplexy

A

Haemorrahge into pituitary adenoma

Acute headache, diplopia, hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GH physiology
- Period when it is highest
- Stimulator and Inhibitor
- MoA

A

Puberty

GHRH stimulates, somostatin inhibits

Binds to receptors on liver, causing dimerisation + phosphorylation and IGF-1 release.
Effects - CHO and fat breakdown, protein buildup

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

Diagnosis of Acromegaly

A

Elevated IGF1? - diagnoses

Equivocal
- OGTT - GH not adequately suppressed

Proceed to pituitary MRI

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

Treatment of acromegaly

A

Somostatin analogues
- Octreotide
- Pasireotide - causes new onset diabetes in 60%

Pegvisomant
- Recombinant GH molecule, prevents receptor dimerisation. Enhances insulin sensitivity

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

Test for GH deficiency

A

Serum IGF1

Equivocal, do provocation tests:
- Macromelin test (grehlin, stimulates GH release)
- GHRH test

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

Treatment prolactinoma

A

Cabergoline - ergot Da receptor agonist

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

A/E of cabergoline

A

Valvular heart disease

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

False positive elevated PRL, without any symptoms (galactorrhoea, amenorrhoea)

A

Macroprolactin - PRL bound to Ig’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Ostoporosis agents
- Prevent breakdown

A

Bisphopsphonate - prevent osteoclast binding and induce apoptosis

Denosumab - RANK-L

SERM’s - inhibit osteoclasts through upregulating OPG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Bone anabolic agents

A

Teriparitide - increase osteoblast activity

Romosozumab -inhibits sclerostin, which inhibits osteoblast formation. Increases osteoblast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Physiology of FGF23
- When released
- Effects
- Klotho

A

Hyperphosphataemia

Decreases phosphate reabsorption
Decreases calcitriol synthesis (reducing intestinal absorption)
Suppresses PTH (suppress vit D)

Klotho is a co-receptor that enhanced FGF23. Depleted in CKD, so reduced efefct of FGF23 in CKD (on kidneys, parathyroid) –> lead to CKD MBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Calcium sensing receptor
- Function
- Defects

A

Senses iCa, increases PTH release in response to low levels

Inactivation - causes familial hypocalcuric hypercalcaemia (excess PTH release as iCa not sensed)

Cincalcet - CasR sensitiser, sensitising to Ca and suppressing PTH release (in CKD-MBD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Bone resorption markers

A

Urine NTX
Serum CTX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Bone formation markers

A

BSAP
PINP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Ca replacement when on PPI

A

Ca citrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Denosumab
- Risk of not taking within 4 weeks

A

Spontaneous vertebral fractures
- Need to take bisphosphonate cover

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Denosumab - cf with bisphosphonates

A

Increased eczema and infection risk

Less renal dose adjustment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Atypical femur fracture
- Presentation
- Management

A

Indolent groin pain whilst on bisphosphonate

Stop bisphopshonate/denosumab immediately and refer to orthopaedic centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Bisphosphonates duration

A

5 years for oral, 3 years for IV

Continue in high risk (Age > 70, low T score, high risk fragility fracture)

Drug holiday for 2-3 years, recheck T score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Phentermine
- MoA
- Use
- A/E

A

Adrenergic agent suppresses appetite

Obesity

Adrenergic A?E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Orlistat
- MoA
- A/E

A

Lipase inhibitor, reduces fat absorption

Steatorrhoea, flatulence, oxalate stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Criteria for bariatric surgery

A

BMI > 40
BMI >35 and failed medical therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pathogenesis of thyroid eye and skin disease

A

TSH receptors and IGF-1 receptors on orbital fibroblasts and skin

Excess TSH stimulates receptors in eye muscles and skin
–> excess GAG secretion, fluid accumulation.
–> Extraocular muscle swelling, proptosis, pretibial myxoedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Specific and non-specific features of Grave’s disease

A

Specific - periorbital oedema, proptosis, conjunctival inflammation

Non-specific - lid lag, stare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Treatment of Grave’s eye disease
- Everyone
- Mod/severe

A

Treat hyperthyroid, stop smoking, conservative with drops

Severe
- steroids
- Teprotumumab - IGF-R inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Thyroid storm
- Features

A

Hyperthyroid

Fever
Tachycardia
CNS - psychosis, seizure, coma
Heart failure
Hepatic dysfuncton

47
Q

MoA of PTU in thyroid storm

A

Blocks T3/T4 synthesis

Blocks peripheral T4 –> T3

48
Q

MoA of Lugol’s iodine in thyroid storm

Remember it is iodine solution

A

Blocks T3/T4 release

49
Q

MoA of Dex in thyroid storm

A

Blocks T4 –> T3 peripherally

50
Q

When to treat hyperthyroidism in pregnancy

A

Graves - TSHRAb positive, as this can cross placenta
- PTU 1st trimester
- Carbimazole other times

Do not treat gestational

51
Q

Episodes muscle weakness
Low K

Cause?
Differentiate from?

A

Hypokalaemia periodic paralysis

Exclude thyroid disease
Exclude Anderson syndrome (ECG for long QT)

52
Q

Test for primary hyperaldosteronism

A

Plasma aldosterone high, plasma renin low. If K low, confirms

Confirmatory tests
- Oral Na load
- Saline suppression
- Fludrocort suppression

53
Q

Phaeo management
- Imaging
- Genetic testing
- Medical

A

MRI/CT ABdo - look for unilateral or b/l

Genetic - vHL, MEN2, can have bilateral

Medical - ALWAYS alpha blocker first

54
Q

AIRE

A

Autoimmune polyendocrine syndrome 1
- adrenal insufficiency

55
Q

Diabetic
Collapse of midfoot/arch
Acute hot, red swollen foot

?cause
?other considerations

A

Charcot’s (diabetic) neuroarthropathy

Charcot’s think midfoot/arch.

Exlude osteomyelitis, gout

56
Q

Management of charcot’s

A

Contact casting/podiatry to offload foot

57
Q

Function of kisspeptin

A

Stimulates GnRH release (remember pulsatile fashion)

58
Q

Requirements for functional GnRH secretion

A

GnRH neurons must migrate appropriately (through olfactor bulb) - error = Kallmans’ syndrome

Must secrete in pulsatile manner - continuous (GnRH agonists) = suppression

59
Q

Pathophys of PCOS

A

Functional ovarian hyperandrogenism -increased sensitivity to LH

Functional adrenal hyperandrogenism

Selective insulin resistance - insulin acts on theca cells to increase androgen synthesis

60
Q

Diagnosis of PCOS

A

Amenorrhoea/oligomenorrhoa

> 20 follicles U/S

High testosterone
- Clinical - hirsuitism
-Elevated testosterone

61
Q

Test for CAH

A

21 a hydroxylase deficiency

Check 17 OH levels - high indicates 21a hydroxylase deficiency

62
Q

Fertility management for PCOS

A

Metformin/weight loss - by 10% can improve fertility

Ovulation induction
- Letrozole, aromatase inhibitor increased ovarian oestrogen

Clomiphene - oestrogen receptor antagonist, increases FSH production

63
Q

Diagnosis of relative energy deficiency (functional hypothalamic amenorrhoae

A

Amenorrhoea

Low FSH, LH and oestradiol

63
Q

Diagnosis of relative energy deficiency (functional hypothalamic amenorrhoae

A

Amenorrhoea

Low FSH, LH and oestradiol

Trigger - eating disorder, excercise, stress

64
Q

Mullerian ducts/structures

A

Uterus
Fallopian tubes
Superior part of vagina
Female external genitalia

65
Q

Male sex development from embroy

A

XY - Y has SRY gene which causes gonad to become testes

Testis produce 3:
- AMH - regress Mullerian ducts
- 5a DHT - male sex characteristics
- testosterone - wollfian ducts

66
Q

Female characteristic development

A

XX - default ovaries produced

Mullerian ducts form –> female sex characteristics

Lack of SRY, or lack of AMH from testis (gonadal dysgenesis) cause female characteristics

67
Q

Female sex characteristics
Normal pubarche, adrenarche
Streak gonads

A

46XY gonadal dysgenesis

68
Q

Amenorrhoea
Female characteristics, absence of hair, adrenarche
46XY

A

Androgen insensitivity syndrome

69
Q

Evaluation of possible primary ovarian insufficiency

A

TSH and PRL - ensure normal

Check FSH, LH, E2 and AMH
- E2 low, FSH and LH high –> likely POI

AMH low also supports diminshed ovarian reserve

70
Q

2 most common causes POI

A

Idiopathic
Autoimmune -APS1 (AIRE)

71
Q

When to use transdermal ostrogen rather than oral

A

Hypertriglyceridaemia
Imapired Liver
Migraine with aura

72
Q

Woman with uterus - formulation for HRT?

A

Combined oestrogen and progesterone

73
Q

Absolute contraindications to HRT

A

ABCD
Acute liver disease
Bleeding - undiagnosed vaginal bleeding
Cancer (rbeast/uterine), Cardiovascular disease
DVT( or thrombophilia)

74
Q

Low test
Low FSH/LH
Anosmia

A

Kallman’s syndrome

Failure of migration of GnRH neurons through olfactory bulb with olfacotry neurons

75
Q

When to treat euvolemic HypoNa with Hypertonic saline

A

Na < 120

Cerebral symptoms - decreased GCS, seizure, headache

76
Q

Inhibitors of growth hormone

A

IGF1
Leptin
Somostain (GHIH)
Hyperglycaemia

LISH

77
Q

High TSH
High T4

A

Heterophile antibody - can interfere with assay

78
Q

Hyperthyroid
No uptake on nuclear scan
TPO positive

DDx?

A

Silent thyroditis - spectrum with Hashimoto’s (progresses to Hashimoto’s with alter hypothyroid)

Postpartum - within 12 months of birth/miscarriage

79
Q

Dequarvain’s thyroiditis Rx

A

NSAIDs first line
Pred 2nd line

BB for symptoms

80
Q

Hypercalcaemia
AKI
Metabolic alkalosis

A

Milk Alkali syndrome

81
Q

Activating mutation of TSH receptor causes?

A

Thyroid adenoma or toxic multinodular goitre

82
Q

Treatment of hypercalcaemia

A

IV fluids ALWAYS 1st line

2nd line - IV bisphosphonate

83
Q

Aldosterone levels in primary vs secondary adrenal insufficiency

A

2nd - usually preserved aldosterone

84
Q

Which fracture site is at greatest risk with steroid osteoporosis?

A

Vertebral

85
Q

High oestrogen, low LH, normal testosterone.

YOung male, gynaecomastia.

Next ix?

A

Suggests aromatisation of testosterone. Can be done by HCG from teste tumour

Testicular U/S

86
Q

Factor greatest effect on peak bone mass?

A

Genetics

87
Q

Osteoporosis men with hypogonadism

A

Treat with testosterone

88
Q

Testosterone changes in obesity

A

Low SBG - inhibition of liver. Causes decrease total testosterone

Increase peripheral conversion by aromatase from testosterone to oestrogen

89
Q

ACTH dependant Cushing’s, no lesion on MRI

Next step?

A

Petrosal sinus sampling - confirm if from pituitary.

Sometimes MRI won’t pick up pituitary adenoma

90
Q

Mechanism of steroid induced osteoporosis

A

Decreased production of OPG

91
Q

Low BSL

Insulin high
C peptide normal

A

Insulinoma

92
Q

MoA of GLP-1 agonists

A

Stimulate glucose dependant secretion of insulin by beta cells

Delay gastric emptying

93
Q

Most specific sign of Cushing’s

Most specific sign in already obese person that points to Cushings

A

Abdominal striae

Proximal myopathy

94
Q

Drug taken with bisphopshonates that reduces absorption

A

CaCO3

95
Q

REsponse to hypogylcaemia in order

A

1) Glucagon

2) Adrenaline

3) Cortisol and GH

96
Q

2nd cause hyperipidaemia most assocaited with increased LDL

A

Hypothyroid

97
Q

Therapy for proliferative diabetes
- First line
- 2nd line

A

1st line - panretinal photocoagulation - best to prevent vision loss

VEGF in short term (until photocoagulation)

2nd line - vitrectomy

98
Q

Therapy for macular oedema

A

Anti-VEGF agents

99
Q

Changes in T2DM

A

1) Impaired glucose tolerance - impaired post prandial

2) Beta cells increase insulin secretion. Can’t keep up
- Increased hepatic GNG causing fasting hyperglycaemia

100
Q

Mechanism of insulin translocating GLUT4 transporter to cell surgace

A

Activating tyrosine kinase receptor on cell surface

101
Q

Steroid induced osteoporosis
- Acute mechanism
- Long term mechanism

A

Acute - decreased OPG, increase RANK-L , increase bone resorption

Long term - decrease bone formation

102
Q

Cushing’s
- Agents that target adrenal

A

KM

Ketoconazole - inhibit androgen synthesis

Metarypone - Stops GC synthesis (inhibit 11b hydroxylase)

103
Q

Cushing’s disease (pituitary)
- Agents that target ACTH
- Agents that target GC receptor

A

PM

ACTH - pasireotide, inhibit ACTH formation

GC receptor - mifepristone

104
Q

Monitor treatment in 2nd hypothyroidism

A

Free T4

105
Q

Causes of increased CBG? (and hence elevated total cortisol)

A

Oestrogen - pregnancy, COCP

Insulin resistance

106
Q

Why take alendronate BEFORE meals

A

Taken with dairy/food, can form mineral complexes

107
Q

Gynacomastia and testicular cancer - cause?

A

bHCG production and direct effect on testicular tissue

108
Q

Bisphosponate associated with impaired bone mineralisation

A

Etidronate

109
Q

Thyroid and PRL
- What causes elevated PRL

A

Hypothyroid

110
Q

TSH receptor AB
- when can treatment for Grave’s be stopped?

A

When TSH r AB low

111
Q

Test to confirm primary adrenal insufficiency

A

Short synacthen (ACTH) test

112
Q

Test to confirm secondary adrenal insufficiency

A

ACTH and cortisol

AND

Synacthen test

113
Q

Sick Euthyroid
- Circumstances
- Labs findings

A

In critically ill patients, functional central hypothyroid to prevent catabolic state

Low T4, low T3, low normal TSH

BPT (18 decks)

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