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Endocrinology Flashcards

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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
Symptoms of GH excess (acromegaly)
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
26
Diagnosis of acromegaly
IGF-1 level (not pulsatile like GH) | Pituitary MRI usually identifies tumour
27
Causes of acromegaly
Pituitary GH-secreting tumour Ectopic GHRH secretion Ectopic GH secretion
28
Management of acromegaly
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
29
Definition of acromegaly
GH excess AFTER fusion of epiphyses | - overgrowth of soft tissues and cartilage
30
Definition of gigantism
GH excess BEFORE fusion of epiphyses - large stature and height Rare (pituitary tumours are rare in childhood)
31
Cushing's disease definition
An excess of cortisol in the body secondary to a pituitary adenoma secreting ACTH
32
Role of dexamethasone suppression test
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)
33
Role of CRH stimulation test in Cushing's syndrome
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
34
Clinical features of hyperprolactinaemia
``` 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) ```
35
Diagnosis of hyperprolactinaemia
Serum prolactin over 5x normal limit
36
Management of pituitary prolactinoma
DA-2 receptor agonists: - bromocriptine, cabergoline - S/E: nausea, postural hypotension, nasal stuffiness
37
Management of secondary hyperthyroidism (i.e. excess TSH secretion from pituitary)
Surgery Radiotherapy OR octreotide (somatostatin analogue)
38
Which are the most common of pituitary adenomas
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
39
Causes of hypopituitarism
``` 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 ```
40
Clinical features of hypopituitarism
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
Management of hypopituitarism
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
Hormones secreted from posterior pituitary
Vasopressin/ADH (water balance) | Oxytocin (suckling reflex)
43
Causes of posterior pituitary disease
Due to posterior pituitary or hypothalamic disease (usually hypothalamic) Tumour or trauma most common
44
Management of central DI
Long-term treatment with desmopressin
45
Zones of the adrenal gland
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
Exogenous glucocorticoids required per day to replace all lost cortisol if there is NO endogenous production
Prednisolone: 5mg/day Hydrocortisone 30mg/day Cortisone acetate 37.5mg/day Dexamethasone 0.5-1mg/day
47
Which glucocorticoid medication is biochemically identical to endogenous cortisone
Hydrocortisone
48
Doses of exogenous corticosteroids at which suppression of HPA axis is likely to occur
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
Definition of phaeochromocytoma
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
Clinical features of phaeochromocytoma
``` 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
Genetic syndrome associated with phaeochromocytoma
MEN2
52
Investigations in phaeochromocytoma
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
Management of phaeochromocytoma
``` Alpha blockade (pehoxybenzamine) Beta blockade (atenolol or metoprolol) Once stable after 1-2 weeks - surgical removal ```
54
Embryological origin of the thyroid gland
Develops from pharyngeal floor (1st and 2nd pharyngeal pouches) in the 3rd week of gestation
55
Cells of the thyroid gland
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
Thyroid hormone ratios, carriage etc.
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
Actions of thyroid hormone
``` 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
Most common cause for hypothyroidism worldwide
Iodine deficiency
59
Most common cause for hypothyroidism in iodine-sufficient areas
Hashimoto's thyroiditis
60
Aetiology of hypothyroidism
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
Clinical features of hypothyroidism
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
Definition of myxoedema coma
A rare life-threatening complication of hypothyroidism characterised by profound lethargy or coma, and usually accompanied by hypothermia
63
Cause of myxoedema coma
Decompensation of hypothyroidism from: - sepsis - exposure to cold - CNS depressants (sedatives, narcotics, antidepressants) - trauma/surgery - stroke, CHF, burns - intravascular volume contractions
64
Management of myxoedema coma
``` Reduce further heat loss ICU monitoring Support respiration as indicated IV hydration IV thyroxine Glucocorticoids (until adrenal insufficiency excluded) Treat precipitating factors ```
65
Definition of Hashimoto's thyroiditis
A chronic autoimmune mediated destruction of the thyroid gland, characterised by gradual thyroid failure due to apoptosis of thyroid epithelial cells
66
Diagnosis of Hashimoto's thyroiditis
``` 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
Types of diabetes medications
``` Biguanides (metformin) Sulfonylureas (glicazide) Thiazolidinediones (pioglitazone) Alpha-glucosidase inhibitor (acarbose) Insulin analogues ```
68
Biguanides: example, mechanism
Metformin Sensitises peripiheral tissues to insulin + Stimulatino of hepatic AMPK - reduced hepatic glucose production
69
Side effects of metformin
GI upset Lactic acidosis Anorexia
70
Contraindications to metformin
``` Liver dysfunction (or alcohol abuse) Renal dysfunction (GFR 30ml/min) Cardiac dysfunction ```
71
Mechanism of sulfonylureas
Glicazide | Blocks K+ channel - depolarisation of beta cells - calcium influx - insulin release
72
Side effects and contraindications of sulfonylureas (glicazide)
Hypoglycaemia weight gain Contraindicated in severe liver dyfunction Do not combine with a non-sulfonylurea or pre-prandial insulin
73
Mechanism of pioglitazone
Inc. peripheral insulin sensitivity from reducing FFA release from adipose
74
Side effects of pioglitazone
Heart failure Oedema Increased fracture risk Increase bladder cancer
75
Contraindications to piioglitazone
Class II or higher congestive heart failure | DO NOT COMBINE WITH INSULIN
76
Mechanism of acarbose
Inhibits brush border alpha- glucosidase - reduced GI absorption of carbohydrates
77
Indication for acarbose
Postprandial hyperglycaemia
78
Side effects of acarbose
Flatulence Abdominal cramps Diarrhoea
79
Contraindications of acarbose
Inflammatory bowel disease | Severe liver dysfunction
80
Anti-thyroid medications
Carbimazole: inhibits iodine and TPO interactions with thyroglobulin Propylthiouracil reduced T4 to T3 conversion in addition to above mechanism
81
Side effects of anti-thyroid medications
``` Nausea/vomiting Rash hepatitis Cholestasis Agranulocytosis ```
82
Contraindications to anti-thyroid medications
renal and liver disease Carbimazole: 1st trimester pregnancy Propythiouracil: 2nd and 3rd trimester pregnancy
83
Recommended 1st and 2nd line oral hypoglycaemic agents
1st: Metformin 2nd: sulfonylureas/DPP-4 inhibitors
84
Which oral hypoglycaemic agent has the highest risk of hypoglycaemic episodes
Sulfonylureas
85
Which oral hypoglycaemic agents have the lowest cost?
Metformin and sulfonylureas
86
Which oral hypoglycaemic agents cause weight loss?
Incretins (exenatide), gliflozins
87
Diabetic medications which cause weight gain:
Insulin, sulfonylureas, glitazone
88
Initial type 2 diabetes management according to HbA1c
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
Mechanism of DDP-4 inhibitors
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
Which oral hypoglycaemic agent has the least side effect profile
DDP-4 inhibitors (gliptins)
91
Example of DDP-4 inhibitor
Gliptins e.g. sitagliptin
92
Mechanism of GLP-1 agonists
Binds to GLP-1 receptor, therefore does not rely on endogenous GLP-1 (more efficacious than DDP-4 inhibitors)
93
Side effects of GLP-1 agonists
``` 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
Example of a GLP-1 agonist
Exenatide
95
Mechanism of SGLT-2 inhibitor
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
Side effects of SGLT-2 inhibitors
Weight loss Genital infections, UTIs Polyuria Volume depletion, reduced blood pressure
97
Contraindications for SGLT-2 inhibitors
GFR less than 60 | Not toxic, just requires a working nephron to exert effect
98
Example of a SGLT-2 inhibitor
Gliflozins (dapagliflozin)

Medicine (12 decks)

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