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Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Endocrine cells of the pancreas and the hormones they secrete

A

Beta-cells: insulin and amylin
Alpha-cells: glucagon
Delta-cells: somatostatin
Gamma-cells: polypeptide of unknown function

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2
Q

Definition of hyperosmolar hyperglycaemic state

A

An acute complication of DM characterised by severe hyperglycaemia with NO ketoacidosis

AKA hyperosmolar non-ketotic state

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3
Q

Precipitants of hyperosmolar hyperglycaemic state

A

Acute major illness (MI, CVA, sepsis, pancreatitis)
Poor compliance
Dehydration

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4
Q

Clinical features of hyperosmolar hyperglycaemic state

A

Insidious development, often over several days
- polyuria
- polydipsia
- weight loss
As increases further:
- neuro symptoms (lethargy, focal signs, reduced alertness)
- progress into coma in late stage

NO HYPERVENTILATION OR ABDO PAIN LIKE IN DKA

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5
Q

Definition of ulcer

A

Break in continuity of the skin penetrating full thickness of dermis

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6
Q

Risk factors for diabetic foot

A 
Diabetic neuropathy
Peripheral vascular disease
Elderly
Deformity
Previous history
Patient living alone
trauma
Other microvascular complications (e.g. CKD, retinopathy)
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7
Q

Definition of hammer toe

A

Fixed deformity with flexion at the PIP joint causing elevation of the PIP joints

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8
Q

Definition of claw toe

A

Fixed extension at MTP joints + flexion at PIP and DIP joints

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9
Q

Definition of mallet toe

A

Flexion deformity of DIP joints (often only affects 2nd digit)

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10
Q

Neurovascular examination of diabetic foot

A

PERFORM AT LEAST 1-2 NEURO and 1-2 VASCULAR TESTS in OSCE

  • Monofilament*
  • Vibration sense* (128Hz)
  • Proprioception*
  • ankle reflex
  • Pin prick
  • Peripheral pulses
  • Doppler USS
  • ABPI
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11
Q

Wound classifications for diabetic foot

A

WAGNER GRADES
I: superficial, not infected
II. Deep ulcer +/- tendon involvement, WITHOUT bone involvement
III: Deep ulcer with tendon and bone involvement
IV: Localised gangrene
V: Complete gangrene

Refer to podiatrist for anything grade II and above!

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12
Q

How to test for bone involvement in an ulcer

A

Probe test - if hits bone = clear path to bone = BONY INVOLVEMENT
Technetium bone scan - good sensitivity, poor specificity
MRI: look for internal involvement (Inx of choice for osteomyelitis)
Foot swab

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13
Q

Methods of reporting ulcer wound

A 
S(AD) SAD:
Size (Area, Depth) of ulcer
Sepsis - is it infected?
Arteriopathy - poor vascular supply?
Denervation - neuropathy?
or
PEDIS
Perfusion: palpable pulsels?
Extent: area
Depth
Infection
Sensation
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14
Q

Management of neuropathic ulcers

A

Control BGL
Smoking cessation
Preparation of wound bed (debridement, treatment of local oedema)
Off-loading = relieving high pressure areas
- Total compact cast/TCC (foot in case, pressure off all critical areas + immobilisation)
- removable casts (strap on and off)
- combination instant cast: removable + POP
Dressing: hydrocolloid, topical silver

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15
Q

Management of foot ingections

A

Antibiotics: Hospital specific broad spectrum protocols
- augmentin/tazocin ususally
- for soft tissue infections: 1-2 weeks
- for osteomyelitis over 6 weeks
Negative pressure wound healing (Vac dressing)
Hyperbaric oxygen (40x 1h sessions_
Larval therapy (green bottle fly larvae)

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16
Q

Definition of Charcot’s foot

A

Non-infective, destructive neuropathic arthropathy occurring in a WELL PERFUSED, insensate foot.

Progressive degenerative arthritis resulting from damaged nerves that leads to progressive deterioration of weight bearing joints, usually foot/ankle

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17
Q

Cause of Charcot’s foot

A

Neurotrauma (due to reduced pain sensation and proprioception) - repetitive mechanical trauma to foot
Neurovascular (dysfunctional blood supply - lax ligaments, microfractures, osteopenia, bone destruction)

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18
Q

Presentation of Charcot’s foot

A 
Atrophic type: "sucked candy cane)
Hypertrophic type
Rockerbottom foot arch (#s - collapse of tarsal bones - outward bowing of arch)
Dislocation/instability of foot
osteophytes
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19
Q

Management of Charcot’s foot

A

Immobilise and offload with total compact cast (TCC)
CROW walker (charcot restraint orthotic walker)
Bespoke shoes with stiffened sole and moulded insoles

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20
Q

Anatomy of anterior pituitary

A

Sits within sphenoid sella turnica
Cavernous sinus laterally (CN III, IV, V1, V2, VI)
Optic chiasm superiorly
Anterior pituitary develops from oral ectoderm (Rathke’s pouch)

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21
Q

Which hormones does somatostatin inhibit at the anterior pituitary

A

Thyrotropin releasing hormone

Growth hormone

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22
Q

Evidence of pituitary hormone excess

A

Acromegaly (GH)
Cushing’s (Cortisol)
Biochemically: IGF-1, prolactin, 24h urinary free cortisol, TSH/Free T4

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23
Q

Evidence of mass effect from pituitary adenomas

A 
Bitemporal hemianopia (optic chiasm)
CN lesions (cavernous sinuses)
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24
Q

Pituitary imaging

A

MRI!
Extensions superiorly to optic chiasm may be discernible
Incidentalomas are quite common - small, non-secreting, do not require treatment
Smaller tumours may be missed (40% of Cushing’s pituitary tumours cannot be seen on imaging)

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25
Q

Symptoms of GH excess (acromegaly)

A

Overgrowth of soft tissues and cartilage:

  • increased ring, shoe and hat size
  • enlargement of nose and jaw
  • underbite (prognathism)
  • increased gap between teeth
  • HTN
  • increased tongue size
  • diabetes mellitus
  • mass effects of pituitary
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26
Q

Diagnosis of acromegaly

A

IGF-1 level (not pulsatile like GH)

Pituitary MRI usually identifies tumour

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27
Q

Causes of acromegaly

A

Pituitary GH-secreting tumour
Ectopic GHRH secretion
Ectopic GH secretion

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28
Q

Management of acromegaly

A

Trans-sphenoidal resection of tumour (80% success rate)
Medical treatment:
- Octreotide (long acting somatostatin analogue)
- Dopamine agonists useful in tumours which also secrete prolactin
- RTx for failed surgery

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29
Q

Definition of acromegaly

A

GH excess AFTER fusion of epiphyses

- overgrowth of soft tissues and cartilage

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30
Q

Definition of gigantism

A

GH excess BEFORE fusion of epiphyses - large stature and height
Rare (pituitary tumours are rare in childhood)

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31
Q

Cushing’s disease definition

A

An excess of cortisol in the body secondary to a pituitary adenoma secreting ACTH

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32
Q

Role of dexamethasone suppression test

A

In ACTH dependent Cushing’s syndrome
Pituitary adenomas secreting ACTH are RELATIVELY resistant to negative feedback by glucocorticoids
Nonpituitary tumours with ectopic ACTH secretion are COMPLETELY resistant to feedback inhibition

i.e. if pituitary dependent, cortisol levels after the dexamethasone suppression will be less than a certain amount (but will be detectable, unlike in healthy patients)

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33
Q

Role of CRH stimulation test in Cushing’s syndrome

A

45 minutes after IV administration of CRH, most patients with Cushing’s disease will respond with increase in ACTH and cortisol
Those with ectopic ACTH-secreting tumours or adrenal tumours do not respond because pituitary ACTH secretion is already suppressed

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34
Q

Clinical features of hyperprolactinaemia

A 
Premenopausal women:
- amenorrhoea
- infertility
- galactorrhoea
- tend to be diagnosed early
In men:
- hypogonadism
- reduced libido
- Impotence
- often diagnosed late with visual change as symptoms are assumed to be caused by other things
In post-menopausal women:
- mass effect only (hemianopia, headaches due to raised ICP)
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35
Q

Diagnosis of hyperprolactinaemia

A

Serum prolactin over 5x normal limit

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36
Q

Management of pituitary prolactinoma

A

DA-2 receptor agonists:

  • bromocriptine, cabergoline
  • S/E: nausea, postural hypotension, nasal stuffiness
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37
Q

Management of secondary hyperthyroidism (i.e. excess TSH secretion from pituitary)

A

Surgery
Radiotherapy
OR octreotide (somatostatin analogue)

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38
Q

Which are the most common of pituitary adenomas

A
  1. non-functioning/gonadotropin secreting tumours
  2. Prolactin secreting tumours (commonest FUNCTIONING tumour)
  3. GH secreting
  4. Cushing’s (ACTH secreting)
  5. TSH secreting tumours can occur but are rare
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39
Q

Causes of hypopituitarism

A 
Most commonly due to pituitary tumour
Past pitutiary Sx or Rtx (50% develop within 4y)
Autoimmune disease
Postpartum lymphocytic hypophysitis
Haemochromatosis
Sheehan's syndrome (following PPH)
Carniopharyngioma
Rare genetic causes
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40
Q

Clinical features of hypopituitarism

A

ACTH/cortisol: hypotension, weight loss, fatigue
TSH: cold intolerance, fatigue
Gonadotropins: loss of menses, libido and shaving
Prolactin: no clinical effects
GH: subtle reduction in exercise tolerance, body composition and metabolism (growth failure in children)

41
Q

Management of hypopituitarism

A

Only TSH and ACTH are essential for life
Replace cortisol: e.g. 20-30mg hydrocortisone/day
Replace thyroid - monitor with serum free T4 (aim for normal range)
Replace sex steroids (OCP or HRT, testosterone via 3 monthly IM injection or daily cutaneous gel)
Replace gonadotropins for fertility
No need to replace prolactin, GH replacement only given in children with growth failure

42
Q

Hormones secreted from posterior pituitary

A

Vasopressin/ADH (water balance)

Oxytocin (suckling reflex)

43
Q

Causes of posterior pituitary disease

A

Due to posterior pituitary or hypothalamic disease (usually hypothalamic)
Tumour or trauma most common

44
Q

Management of central DI

A

Long-term treatment with desmopressin

45
Q

Zones of the adrenal gland

A

Cortex (90% - mesodermal origin - steroid hormones)
Zona glomerulosa: mineralocorticoids (aldosterone) - retains salt
Zona fasciculata: glucocorticoids (cortisol)
Zona reticularis: androgen/sex hormones (DHEA - testosterone, oestrogen)

Medulla (10% - derived from neural crest cells - catecholamines)

  • Adrenaline
  • Noradrenaline
  • Dopamine
46
Q

Exogenous glucocorticoids required per day to replace all lost cortisol if there is NO endogenous production

A

Prednisolone: 5mg/day
Hydrocortisone 30mg/day
Cortisone acetate 37.5mg/day
Dexamethasone 0.5-1mg/day

47
Q

Which glucocorticoid medication is biochemically identical to endogenous cortisone

A

Hydrocortisone

48
Q

Doses of exogenous corticosteroids at which suppression of HPA axis is likely to occur

A

Over 10mg/day prednisolone for over one month
(1.5-2x replacement dose)
i.e. unlikely to occur following short courses for asthma etc,
Almost certainly will occur for temporal arteritis, transplant rejection treatment etc

49
Q

Definition of phaeochromocytoma

A

Tumour arrising from chromaffin cells in the sympathetic nervous system (usually in the adrenal medulla) that secrete any combination of adrenaline and/or noradrenaline and occasionally dopamine

50
Q

Clinical features of phaeochromocytoma

A 
Episodic/paroxysmal in 50%
- HTN
- headaches
- sweating
- anxiety/fear
- nausea, vomiting
- chest, abdo pain
Between episodes (not experienced by all patients)
- cold hands/feet
- weight loss
- hyperglycaemia or hypo
- postural hypotension
51
Q

Genetic syndrome associated with phaeochromocytoma

A

MEN2

52
Q

Investigations in phaeochromocytoma

A

Elevated catecholamines in blood and urine (3-4x upper limit of normal at LEAST)
Plasma free metanephrines (metabolites of adrenaline)
Clonidine suppression test if equivocal results
CT/MRI of adrenals

53
Q

Management of phaeochromocytoma

A 
Alpha blockade (pehoxybenzamine)
Beta blockade (atenolol or metoprolol)
Once stable after 1-2 weeks - surgical removal
54
Q

Embryological origin of the thyroid gland

A

Develops from pharyngeal floor (1st and 2nd pharyngeal pouches) in the 3rd week of gestation

55
Q

Cells of the thyroid gland

A

Follicular cells: secrete thyroid hormone (mainly T4/thyroxine)
Follicles filled with colloid stores thyroid hormone

Parafollicular cells: secrete calcitonin (only significant in times of high calcium demand i.e. breastfeeding, pregnancy)

56
Q

Thyroid hormone ratios, carriage etc.

A

93% T4/thyroxine

  • mostly converted to T3 in tissues
  • higher binding protein affinity (10x half-life of T3)

7% T3/triiodothyronin
- 4x as potent as T4 (higher affinity for receptors)

Over 99% is protein-bound in plasma (thyroxine-binding globulin, albumin)

57
Q

Actions of thyroid hormone

A 
Metabolic rate and metabolism:
- inc. heat production
- inc. O2 consumption
- inc. lipolysis
- inc. glycogenolysis
Cardiovascular
- inc. contractility
- inc. cardiac output
Sympathetic effects:
- inc. beta receptors - inc. catecholamine permissive actions
- red. a receptors
Gastrointestinal:
- inc. gut motility
Growth effects:
- permissive for GH synthesis, secretion and action
- important in development of CNS
58
Q

Most common cause for hypothyroidism worldwide

A

Iodine deficiency

59
Q

Most common cause for hypothyroidism in iodine-sufficient areas

A

Hashimoto’s thyroiditis

60
Q

Aetiology of hypothyroidism

A
  1. Primary: thyroid failure (90%)
    - Hashimoto’s
    - Iatrogenic (Li, RTx, Tx for hyperthyroid)
    - Infiltrative (amyloid)
    - Iodine deficiency
    - Congenital
  2. Secondary: pituitary deficit of TSH
    - adenomas or destruction
  3. Tertiary: hypothalamic deficit of TRH
    - rare, also adenomas/destruction
  4. Peripheral resistance to hormone
61
Q

Clinical features of hypothyroidism

A

Psych: mental sluggishness, psychosis, confusion
Eyes: puffy
ENT: deafness, hoarseness
Skin: dry, alopecia
Rheum: myalgia, arthralgia, proximal myopathy
Heart: HF, hypotension, bradycardia
GIT: constipation
Metabolic: intolerance to cold, weight gain, red. appetite
GYN: menorrhagia
Haem: anaemia
Neuro: coma, carpal tunnel

62
Q

Definition of myxoedema coma

A

A rare life-threatening complication of hypothyroidism characterised by profound lethargy or coma, and usually accompanied by hypothermia

63
Q

Cause of myxoedema coma

A

Decompensation of hypothyroidism from:

  • sepsis
  • exposure to cold
  • CNS depressants (sedatives, narcotics, antidepressants)
  • trauma/surgery
  • stroke, CHF, burns
  • intravascular volume contractions
64
Q

Management of myxoedema coma

A 
Reduce further heat loss
ICU monitoring
Support respiration as indicated
IV hydration
IV thyroxine
Glucocorticoids (until adrenal insufficiency excluded)
Treat precipitating factors
65
Q

Definition of Hashimoto’s thyroiditis

A

A chronic autoimmune mediated destruction of the thyroid gland, characterised by gradual thyroid failure due to apoptosis of thyroid epithelial cells

66
Q

Diagnosis of Hashimoto’s thyroiditis

A 
Raised autoantibodies:
- thyroglobulin antibodies (TgAb)
- thyroid peroxidase antibodies (TPO)
- TSH receptor inhibiting antibodies
Iodine N
Thyroid imaging:
- reduced uptake on radioactive iotine uptake scan
67
Q

Types of diabetes medications

A 
Biguanides (metformin)
Sulfonylureas (glicazide)
Thiazolidinediones (pioglitazone)
Alpha-glucosidase inhibitor (acarbose)
Insulin analogues
68
Q

Biguanides: example, mechanism

A

Metformin
Sensitises peripiheral tissues to insulin
+
Stimulatino of hepatic AMPK - reduced hepatic glucose production

69
Q

Side effects of metformin

A

GI upset
Lactic acidosis
Anorexia

70
Q

Contraindications to metformin

A 
Liver dysfunction (or alcohol abuse)
Renal dysfunction (GFR 30ml/min)
Cardiac dysfunction
71
Q

Mechanism of sulfonylureas

A

Glicazide

Blocks K+ channel - depolarisation of beta cells - calcium influx - insulin release

72
Q

Side effects and contraindications of sulfonylureas (glicazide)

A

Hypoglycaemia
weight gain

Contraindicated in severe liver dyfunction
Do not combine with a non-sulfonylurea or pre-prandial insulin

73
Q

Mechanism of pioglitazone

A

Inc. peripheral insulin sensitivity from reducing FFA release from adipose

74
Q

Side effects of pioglitazone

A

Heart failure
Oedema
Increased fracture risk
Increase bladder cancer

75
Q

Contraindications to piioglitazone

A

Class II or higher congestive heart failure

DO NOT COMBINE WITH INSULIN

76
Q

Mechanism of acarbose

A

Inhibits brush border alpha- glucosidase - reduced GI absorption of carbohydrates

77
Q

Indication for acarbose

A

Postprandial hyperglycaemia

78
Q

Side effects of acarbose

A

Flatulence
Abdominal cramps
Diarrhoea

79
Q

Contraindications of acarbose

A

Inflammatory bowel disease

Severe liver dysfunction

80
Q

Anti-thyroid medications

A

Carbimazole: inhibits iodine and TPO interactions with thyroglobulin

Propylthiouracil reduced T4 to T3 conversion in addition to above mechanism

81
Q

Side effects of anti-thyroid medications

A 
Nausea/vomiting
Rash
hepatitis
Cholestasis
Agranulocytosis
82
Q

Contraindications to anti-thyroid medications

A

renal and liver disease

Carbimazole: 1st trimester pregnancy
Propythiouracil: 2nd and 3rd trimester pregnancy

83
Q

Recommended 1st and 2nd line oral hypoglycaemic agents

A

1st: Metformin
2nd: sulfonylureas/DPP-4 inhibitors

84
Q

Which oral hypoglycaemic agent has the highest risk of hypoglycaemic episodes

A

Sulfonylureas

85
Q

Which oral hypoglycaemic agents have the lowest cost?

A

Metformin and sulfonylureas

86
Q

Which oral hypoglycaemic agents cause weight loss?

A

Incretins (exenatide), gliflozins

87
Q

Diabetic medications which cause weight gain:

A

Insulin, sulfonylureas, glitazone

88
Q

Initial type 2 diabetes management according to HbA1c

A

less than 7.5: lifestyle modification + metformin - follow up in 3 months

7.5 - 9%: metformin + SU/DDP-4i/insulin

Greater than 9% (OR symptomatic hyperglycaemia) - concern about relative insulin deficiency therefore start insulin immediately (+metformin)

89
Q

Mechanism of DDP-4 inhibitors

A

DDP-4 is an enzyme which cleaves endogenous GLP-1 so that is has a very short half-life. Therefore by inhibiting this enzyme, inhibit cleavage, increases half-life of GLP-1 (increases secretion of insulin, inhibits secretion of glucagon)

90
Q

Which oral hypoglycaemic agent has the least side effect profile

A

DDP-4 inhibitors (gliptins)

91
Q

Example of DDP-4 inhibitor

A

Gliptins e.g. sitagliptin

92
Q

Mechanism of GLP-1 agonists

A

Binds to GLP-1 receptor, therefore does not rely on endogenous GLP-1 (more efficacious than DDP-4 inhibitors)

93
Q

Side effects of GLP-1 agonists

A 
Red. gastric emptying (early satiety, red. appetite, nausea in 50%[usually improves])
Weight loss (more than SGLT2-i)
- 1/3 over 5% weight loss
- 1/3 less than 5%
- 1/3 no effect on weight

Long term use - down regulation of receptors - reduced efficacy over time

94
Q

Example of a GLP-1 agonist

A

Exenatide

95
Q

Mechanism of SGLT-2 inhibitor

A

Inhibits co-transport of Na/glucose in PCT of nephron - inhibits reabsorption of glucose in PCT - reduced tubular renal threshold for glycosuria - glycosuria at lower glucose concentration

96
Q

Side effects of SGLT-2 inhibitors

A

Weight loss
Genital infections, UTIs
Polyuria
Volume depletion, reduced blood pressure

97
Q

Contraindications for SGLT-2 inhibitors

A

GFR less than 60

Not toxic, just requires a working nephron to exert effect

98
Q

Example of a SGLT-2 inhibitor

A

Gliflozins (dapagliflozin)

Medicine (12 decks)

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