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MD2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Triggers for DKA

A 
New onset T1DM
Infection
Inadequate insulin
Surgery
MI
Pancreatitis

Drugs (Corticosteroids and thiazides, antipsychotics)

Chemotherapy

Psychosocial (EtOh, illicit substance use, eating disorders)

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2
Q

3 criteria for diagnosis of DKA

A

Hyperglycaemia
Ketonaemia
Acidaemia (from ketones)

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3
Q

What is DKA?

A

Occurs in diabetics - excessive serum glucose can’t be taken up into cells due to lack of insulin, so body is essentially starved and burns fats to produce energy which produces ketones as byproduct (acetone, gives fruity breath)

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4
Q

Symptoms of DKA?

A 
Polydipsia, polyuria
\+/-nausea, vomiting; 
leathery, anorexia;
Altered conscious state/confusion, drowsiness;
diffuse abdominal pain

Kussmaul hyperventilation (deep breathing)

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5
Q

What effect does DKA have on serum K?

How do you treat this?

A

Serum K may appear high despite an actual total body K loss. This is due to K shift out of cells into the serum due to insulin deficiency, and a large part of this shifted K is lost in the urine + vomiting can lose K + ketoacids are excreted in urine along with Na/K.
If K is low, add KCl to saline fluid bags.

K may also be normal or high. If high, do not give KCl in saline. Normal saline will cause K to be taken up into cells, as will insulin.

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6
Q

What effect does DKA have on plasma na?

How to manage this?

A

NA tends to be low due to the dilutional effect of water shifting from intra to extracellular space. However, water is lost in large amount in the urine due to polydipsia, which counter acts the dilution effect, so hyponatraemia tends to be mild

Give lots of 0.9% saline fluid (2 large bore cannulas) -> will cause Na to rise as fluid is taken up into cells

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7
Q

Management for Ketoacidosis

A
  1. Resus (ABC)
  2. Fluid (IV Saline)
  3. Electrolytes (K) - if K initially low, replace K before giving insulin because insulin will cause K to move into cells and the K will become even lower. If K normal, give at same time as insulin. If K high, do not give K but monitor it hourly.
  4. Insulin (causes K to move into cells)
  5. 5% Dextrose/glucose if
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8
Q

What electrolytes may need to be replaced in DKA?

A

K
Bicarb
Phosphate

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9
Q

Hyperglycaemic hyperosmolar state

Definition

A

Higher mortality risk and rarer than DKA.

HHS most commonly occurs in elderly patients with type 2 DM who have some concomitant illness that leads to reduced fluid intake. Infection is the most common preceding illness, but many other conditions can cause altered mentation, dehydration, or both.

HHS is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis

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10
Q

Hyperglycaemic hyperosmolar state

SX/signs

A 
Severe hyperglycaemia
Blood osmolarity high
Profound dehydration
Minimal ketosis or KA
Depressed sensorium/coma (neurological deficits)
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11
Q

Hyperglycaemic hyperosmolar state

Treatment

A

Hypo-osmolar saline (0.45% rather than 0.9%)
Insulin
K
Monitor urine output and CVP if indicated
Prophylactic heparin

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12
Q

Treatment of hypoglycaemia

A

If conscious: oral fluids containing sugar or glucogel

If unconscious: 1mg IM/SC glucagon or IV 50% dextrose

Followed by oral carbs (sandwich) when conscious

Reassess glucose 20-30min later

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13
Q

Reason for hypoglycaemic incidence

A 
Too little to eat
Too much insulin
Too much exercise
Other medications (sulfonylureas)
Renal failure
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14
Q

How to avoid hyper/hypoglycaemic emergency

A

DKA/HHS:

  • never omit long-acting insulin (lantus, levemir), if you are T1
  • Education re management when sick (monitor ketones, supplemental short-acting insulin regimes) -> T1D usually need more insulin than usual when unwell

Hypo:

  • always carry form of sugar on you (lollies, juice, jellybeans)
  • appropriate adjustment of glucose lowering therapies to prevent it happening again
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15
Q

investigations to perform for foot ulcer

A

Swab for MCS
Ankle brachial index
Basic bloods (WCC, CRP) +/- blood cultures
XR foot (exclude osteomyelitis)
Doppler USS and/or CT angiogram lower legs

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16
Q

Examination - foot ulcer

A

Colour
Temperature
Cap refill
Palpate pedal pulses and popliteal pulses (?femoral a stenosis)
Describe ulcers - borders, colour, exudate
Probe to bone (bone exposure indicates osteomyelitis)

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17
Q

Management of diabetic foot ulcer

A 
Wound care and dressings
Podiatry
IV antibiotics
Surgical debridement
Reduce weight bearing forces
Tight glycemic control!
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18
Q

Causes of hypothyroidism

A

Primary:
- Autoimmune (hashimoto’s)

  • Iatrogenic (due to I^131, thyroidectomy, external irradiation of neck)
  • Drugs (I, contrast, amiodarone, Li antithyroid drugs)
  • Congenital (absent thyroid, dyhormonogenesis)
  • Dietary I deficiency

Transient:
- post partum thyroiditis
- subacute thyroiditis
- withdrawal of thyroxine treatment

Secondary:

  • Hypopituitarism
  • Hypothalamic disease
  • TSH deficiency/inactivity
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19
Q

What tests should be done to investigate thyroid function?

A

Blood TSH (if high, confirm T4)

Consider thyroid US if palpable goitre

Anti-TPO and Anti-TG antibodies (hashimoto)

Anti-TSH (Graves)

DO NOT need nuclear scan (unless they are thyrotoxic or have solitary nodule on U/S and want to know if it is hot or cold)

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20
Q

Treatment for hypothyroid

A

Thyroxine (needs to be taken separately from Iron, Ca, antacids which decr T4 absorption)

Adequate dietary Iodine

recheck TFTs after 6 weeks and adjust t4 dose if necessary

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21
Q

Causes of hyperthyroidism

A
  • Graves
  • Toxic nodular goitre (multinodular or solitary adenoma)
  • Iodine induced (radiographic contrast, amiodarone)
  • Factitious (too much T4 med)
  • Transient (thyroiditis)
  • Hypersecreting tumour within thyroid
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22
Q

What genes is T1DM linked with?

A

HLAD3 and D4

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23
Q

Pathophys of T1DM

A

Autoimmune destruction of insulin-secreting pancreatic beta cells, requiring patients to take exogenous insulin

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24
Q

What antibodies are associated w T1DM?

A

Islet beta cell antibodies (ICA)

Anti-glutamic acid decarboxylase (GAD)

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25
Q

Micro and macrovascular complications of DM

A

Micro: retinopathy, nephropathy (peripheral and autonomic), neuropathy

Macro: accelerated and more severe atherosclerosis, PVD, CVD (MI) and stroke

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26
Q

What is the upper limit of normal for HBA1C

A

6.5%

Consider less tight control in patients prone to hypoglycaemia (falls in elderly)

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27
Q

What is the diagnostic criteria for DM?

A

Symptoms of hyperglycaemia AND raised venous glucose detected once.

OR Raised venous glucose detected on 2 separate occasions

OR HBA1C > 6.5%

Diabetic if:

  • fasting venous glucose > 7mmol/L
  • random >11.1mmol/L

Impaired tolerance if
fasting glucose 6.1-7

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28
Q

What medical conditions can cause diabetes? What drugs?

A

Medical:

  • Cushings
  • Pheochromocytoma
  • Hyperthyroid
  • Pregnancy

Drugs

  • Steroids
  • Thiazide diuretics
  • Anti-psychotics
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29
Q

MX of T1D

A
  • Education
  • Insulin (pump)
  • Exercise: low intensity aerobic
  • Diet (low GI - small regular meals throughout day)
  • Yearly follow up for presence of complications: Retinal exam, PVD, urinary A:C spot test
  • Monitoring: BSLs and HBA1C
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30
Q

Surgical options of T1D

A
  • Islet cell transplantation into portal vein (protection from autoimmune destruction)
  • Pancreatic transplant
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31
Q

Management of T2D

A

1st line: lifestyle modification

  • Diabetic education programme
  • RF modification: smoking, alcohol, statin, BP control
  • Diet: low GI, low calorie low carb diet
  • Exercise: low intensity aerobic

Medications +/- insulin

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32
Q

What does the HBA1C reflect and indicate?

A

reflects mean glucose level over previous 8 weeks

directly related to risk of complications

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33
Q

What is the first sign of nephropathy in a diabetic?
What test would you perform to detect this?

Management of nephropathy

A

First sign is microalbuminuria -> elevated Albumin: creatinine ratio (A:C spot urine test) but no protein so isn’t picked up on dipstick

MX: ACE inhibitor or ARB (Sartan)

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34
Q

What is insulin glargine? what is the trade name

which types of DM?

A

Lantus - long acting basal insulin with one peak only.

types 1 and 2. take once/ day

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35
Q

What are brand names for rapid acting insulin?

When do you give this?

A

HUmulin and Actrapid

Give 30min before meal

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36
Q

Mixed insulin: how often do you give it and in what cases would you use this?

A

Give it twice daily at breakfast and dinner

Good for people who are low-pre meal and high post meal

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37
Q

Brand names for ultra rapid insulin. When do you take this?

A

Homalog and Novarapid

Take it immediately before eating - onset of action is within 15 min.

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38
Q

What is first line medication for DM?

Mechanism?

SE?

CI?

A

Biguanides (Metformin)

Mechanism: incr insulin sensitivity and decr liver gluconeogenesis

SE: Nausea, diarrhoea

CI: renal failure (eGFR<36)

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39
Q

What Diabetic medications can cause hypos and weight gain?

A

Sulfonylurea causes both

Glitazones (thiaz.) causes weight gain

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40
Q

What happens if metformin isn’t controlling the BSLs adequately?

Then if still high after that, then what?

A
  1. ADD Sulfonylurea (unless BMI>35 then use gliptins which are weight losing)
  2. If still high, oral triple therapy: add Glitazone, gliptin, acarbose, or a long-acting (basal) or pre-mix insulin
  3. add a pre-meal time insulin
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41
Q

What is the mechanism of action of Gliptins?

A

Prologues GLP-1 action
Increases insulin release from beta cells and inhibits glucagon which decreases gluconeogenesis

Decreases gastric emptying to decrease appetite

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42
Q

What diabetic medications are weight losing?

A

Gliptins (decr gastric emptying to incr satiety)

SGLT2 inhibitors increase glucose excretion in renal tubules so you pee out glucose

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43
Q

What are the stages of diabetic eye disease?

A

Non-proliferative

Proliferative retinopathy

Maculopathy

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44
Q

Features of non-proliferative retionpathy

A
  1. Micro aneurysms
  2. Blot haemmhorages
  3. Hard exudates (lipid deposits)
  4. cotton wool spots (infarcts)
  5. Venous beading
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45
Q

Features of proliferative retinopathy

A
  • Neovascularisation due to local hypoxia and ischaemia (new vessels are abnormally frail and grow in wrong places)
  • Large vitreal haemmhorages from new vessels -> VISION LOSS
  • Glaucoma from neovasc.
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46
Q

Features of maculopathy

A

VISION LOSS due to retinal detachment

  • new vessels proliferate, bleed, fibrose
  • fibrosis can pull on retina, resulting in detachment
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47
Q

What is the mechanism of action of Thiazolidinedones (glitazones)

A

Increase insulin sensitivity in muscle and adipose tissue to increase glucose uptake.

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48
Q

What is the concept of a pre-mix insulin?

A

Medium acting + rapid/ultrarapid

49
Q

what pathological feature defines diabetic glomerulosclerosis on histopath?

A

Kimmelstiel wilson nodules

Pink hyaline nodule in mesangium of glomeruli

50
Q

What impact does diabetes have on the eye?

A

Retinal ischaemia and haemmhorage, retinal detachment-> blindness

Glaucoma

Early onset cataracts

CNIII palsy due to infarct

51
Q

Clinical features of diabetic peripheral neuropathy

A

® Injury or infection over pressure points
® Decr sensation in “glove and stocking” pattern
® Absent ankle jerks
® Neuropathic deformity (Charcot joint)

52
Q

What is the character of a neuropathic ulcer and what can this lead to com,plication-wise?

A

Typically painless punched out ulcer in area of thick callus +/- superadded infection

Causes cellulitis, abscess +/- osteomyelitis

53
Q

How to assess for diabetic ischaemic peripheral arterial disease?

A

Doppler +/- angiography

ABI, Buerger’s test
Pulses, temp, cap refill etc

54
Q

Mechanism of action of acarbose

A

alpha glucosidase inhibitor (brush border enzyme ) - decreases carb absorption

55
Q

What is Whipple’s Triad?

A

Refers to diagnosis of hypoglycaemia:

  1. Serum glucose <2.5mM
  2. Neuroglycopenic SX (dizziness, headache, blurred vision, fatigue, confusion, seizures, coma)
  3. Rapid relief provided by administration of glucose
56
Q

MX of hypoglycaemia

A

If conscious: oral fluids containing sugar, followed by longer acting CHO (sandwich)

If unconscious: IM/SC glucagon or IV 50% dextrose

Recheck BSL 20-30min later to see if further treatment required

57
Q

Diabetic renal complications (4)

How do you screen for these?

A
  1. Diabetic glomerulosclerosis - glomerular capillary BM thickening (kimmelstiel wilson nodules)
  2. Papillary necrosis in T1DM (ischaemic necrosis of medullary papillary -> debris may obstruct ureter and present as renal colic +/- hydronephorosis)
  3. Accelerated atherosclerosis in renal arteries -> activates RAAS due to decr blood flow -> incr BP
  4. Autonomic nephropathy (urinary retention -> pyelonephritis)

Screen:

  1. UEC (eGFR and creatinine) and spot urine (A:C ratio)
  2. dipstick if overt nephropahy with macroalbuminuria
58
Q

MX of diabetic retinopathy

A
  1. Glycemic control and BP control
  2. Pan-retinal photocoagulation- burns peripheral retina to decr VEGF production but sacrifices peripheral vision
  3. Vitrectomy (for non-clearing vitreous haemorrhage and retinal detachment)
  4. intravitreal injection of corticosteroid or anti-VEGF
59
Q

What to ask about when inquiring about autonomic neuropathy?

A

Dizziness on standing (postural hypotension)

Sexual function

Faecal incontinence

Nausea after eating (gastroparesis)

60
Q

MX of diabetic neuropathy

A

Glycemic and BP control

Neuropathic pain medications (TCA, Pregabalin, gabapentin, duloxetine)

Foot care education, podiatry

Gastroparesis - metaclopramide

Medical/mechanical/surgical treatment for erectile dysfunction

61
Q

Basic functional roles of the thyroid hormones

A

Metabolism

  • Incr metabolic rate and o2 consumption
  • Calorigenic, heat producing
  • Sympathomimetic: incr HR and CO

Normal development of NS in infants, before and after birth (interacts w GH and IGF secretion)

62
Q

Thyroid hormone synthesis

A

○ Iodine from diet pumped into thyroid follicular cell and then into colloid, and is required for synthesis of T3 and T4
○ Enzymes add I to tyrosine to make T3 (1xI) and T4/thyroxine (2xI)

§ T3: more potent than T4 but 80% is derived from T4

§ T4: more abundant but less potent than T3
T3 and T4 added to thyroglobulin which is taken back into follicular cells where they are separated from Tg and free T3 and T4 can then enter circulation

63
Q

What is the feedback pathway of TH production

A

Hypothalamus -> TRH

TRH via HHPS to anterior pituitary

Anterior pituitary -> TSH

TSH -> Thyroid gland -> T3 and T4

T3 and T4 neg feedback onto anterior pituitary and hypothalamus to suppress TSH and TRH production

64
Q

what hormones does the anterior pituitary produce?

A 
prolactin
GH
TSH
ACTH
LH and FSH
65
Q

What causes a goitre?

What may the presentation be?

A

Increased stimulation of TSH-receptors on the thyroid

may be hypothyroid, hyperthyroid or euthyroid

66
Q

What are the 3 main causes of thyroid disease

A

inflammatory

developmental/congenital (mother who is Iodine deficient)

neoplastic

67
Q

What is a primary cause of hypothyroid?

What is the underlying pathophys and histology?

What blood tests would you do?

Goitre or no goitre?

A

“HASHIMOTO DISEASE”

  • Autoimmune condition, T cell mediated (T4HS)
  • Formation lymphoid follicles, germinal centres with mononuclear inflammatory infiltrate and hurthle cells
  • Chronic inflammation, fibrosis/ scarring
  • F>M
  • Anti-Thyroglobulin and anti-TPO Abs
  • T4 decrease and TSH increase

• Thyroid initially enlarges due to lymphocytic infiltration and fibsosis rather than hypertrophy, then atrophies over time

68
Q

What are 2 primary causes of hyperthyroid?

  • What is the pathophys?
  • What would you see on bloods?
A

GRAVES DISEASE

  • Autoimmune condition , B-cell (Ab) mediated (T2HS)
  • F>M
  • Production of thyroid-stimulating Igs (STIs) from B cells stimulate TSH receptors on thyroid -> trophic effects on thyroid -> diffuse GOITRE and increased T3, T4
  • Incr T3, T4 -> neg feedback -> lower TRH, TSH

HYPERSECRETING TOXIC MULTINODULAR GLANDS

• Nodules of hyper-plastic follicles become autonomous and start secreting T3 and T4

69
Q

What signs are highly specific of graves disease?

A

Signs: oxopthalmus, pretibial myxoedema

70
Q

congenital cause of hypothyroidism

A

mOther who is iodine deficient most commonly

71
Q

What is cretinism?

A

hypothyroid from birth, causes dwarfism and severe mental retardation

72
Q

Cause of a diffuse non-toxic goitre.

what would TFTs show?

A

Dietary iodine deficiency -> T3 and T4 cannot be made -> pos feedback to increase TSH and TRH -> diffuse non-toxic GOITRE (but T3 and T4 remain low no matter how much TSH is present)

73
Q

Secondary cause of hyperthyroidism

Goitre or no goitre in this condition?

What would you see with TFTs?

A

Hypothalamic or anterior pituitary excess (tumour) drives TRH and TSH production -> TSH has trophic effect on thyroid -> GOITRE and increased T3, T4
-> neg feedback from incr T3, T4 unable to suppress excess TRH, TSH

74
Q

Treatment for hyperthyroid

A

Surgery (risks damage to Recurrent laryngeal nerve and parathyroid)

FNA - assess for malignancy if suspected

Radioactive iodine^131 ablation (beta waves)

Drugs: carbemazole

Beta blockers treat SX from sympathetic overdrive

75
Q

what would you see on bloods with subclinical hypothyroid?

What about subclinical hyperthyroid?

Do anything about it?

A

(compensated)
Hypo:
TSH high and T4 normal
No treatment

Hyper:
TSH low and T4 normal
YES because incr risk of AF and stroke! Treat w carbimazole

76
Q

What conditions would light up on a technician scan of the thyroid?

What wouldn’t?

A

POSITIVE:
- Toxic multi nodular goitre (patches)

  • Graves (diffusely lights up)
  • Single solitary nodule (toxic adenoma)

NEGATIVE:

  • Post partum thyroiditis
  • Viral thyroiditis (tender)
  • Amiodarone induced
  • Iodine (contrast etc)
  • Too many T4 pills
77
Q

Clinical présentation of hypoglycaemia

A
  1. Autonomic symptoms from sympathetic overdrive
    - sweaty, anxious, tremor, tachycardia, palpitations, dizziness

.2 Neuroglycopenic symptoms (similar to intoxication/psychosis)

  • confusion, incoherence
  • drowsiness
  • visual trouble
  • seizures
  • coma
78
Q

Causes of hypoglycaemia

A

Diabetic: insulin or sulfonylurea treatment

non-Diabetic: EXPLAIN

Exogenous drugs (alcohol, insulin/other oral hypoglycaemic)

Pituitary insufficiency

Liver failure (no gluconeogenesis)

Addison’s disease (no cortisol)

Islet cell tumours (insulinoma)

Non-pancreatic neoplasms (fibrosarcoma, haemangiopericytoma)

79
Q

Investigations for hypoglycaemia

A

Fingerpick or lab glucose (BSLs)

Insulin, C-peptide (represents endogenous insulin production) and plasma ketones

ABG

80
Q

List causes of adrenal insufficiency.

Primary and secondary

A
  1. Primary causes:
    - Addison’s (autoimmune) most commonly
    - Tb infection (endemic areas)
  • Metastatic cancer
  • Drugs
  • ADrenal haemmhorage
  • Congenital adrenal hyperplasia
  1. Secondary:
    - Withdrawal of exogenous steroids (chronic steroid use suppresses the pituitary adrenal axis)
81
Q

Clinical features of addison’s disease

A
  1. ‘tanned’ skin/palmar creases/extensor surfaces (cross reaction of ACTH w melanin Rs)
  2. GI SX:
    Weakness, fatigue, weight loss, flu-like myalgia and arthralgia, N and V, abdo pain, diarrhoea
  3. Hypotensive w postural dizziness (due to salt wasting)
    - Hyperkalaemia, hyponatraemia, metabolic acidosis
82
Q

What investigations would you do to diagnose Addison’s

A
  1. Bloods: UEC (K, Na), BSL (low), plasma renin and aldosterone
  2. Serum ACTH (high) and cortisol (low) or 24 hour urinary cortisol
  3. ACTH stimulation test: low plasma cortisol levels before ACTH low, and if Addison’s will remain low after ACTH
  4. 21 hydroxylase adrenal autoantibodies (>80% Addison’s)
  5. CT or MRI of adrenals (enlarged if infiltrated or calcified if Tb)
83
Q

Treatment of Acute addison’s disease, then maintenance theraepy

A

Acute:
2-3L IV normal saline (+dextrose if low glucose)
IV Hydrocortisone w gradual tapering
correct any precipitating factors

Maintenance:
-Hydrocortisone (GC) and fludrocortisone (MC) daily

84
Q

Treatment of Acute addison’s disease, then maintenance theraepy

A

Acute:
2-3L IV normal saline (+dextrose if low glucose)
Hydrocortisone w gradual tapering
correct any precipitating factors

Maintenance:
-Hydrocortisone (GC) and fludrocortisone (MC) daily

85
Q

Hormones produced by posterior pituitary and their functions

A

Oxytocin -> Milk ejection and uterus myometrium contraction during labour

Vasopressin/ADH -> incr resorption of water in collecting duct to decrease urine volume

86
Q

Functions of GH

A

Metabolic
- Incr blood glucose and FA

Soft tissues and skeleton
- Growth

IGF production from liver
- does the same thing as GH

87
Q

What conditions result from:

  1. GH deficiency
  2. GH over-secretion
A
  1. Deficiency
    - Dwarfism (decr GH as child)
    - Laron dwarfism = GH insensitivity (GH levels normal but receptors don’t respond)
    - Adult onset dwarfism has few effects
  2. Over-Secretion
    - Gigantism (incr GH before puberty before growth plates have sealed)
    - Acromegaly (incr GH in adulthood leading to bone and soft tissue deformity and incr viscera size)
88
Q

What is another term for GH?

What inhibits GH production in the negative feedback pathway?

A

GH = Somatotropin

Somatostatin is inhibitory

89
Q

What hormones does the adrenal gland produce and from what part of the gland?

what are the disease states of both.

A
  1. Cortex (outer) - > glucocorticoids and mineralocorticoids (aldosterone) and some sex steroids (androgens, oestrogen’s)

Disease state: Cushing’s and addison’s (too much and too little cortisol)
-Androgenital syndrome (too much androgen and oestrogen)

  1. Medulla (middle) - > catecholamines

Disease state: pheochromocytoma (too much adrenaline)

90
Q

Cushing’s syndrome

Clinical

A

□ Hyperglycaemia (diabetes)
□ Hypertension (salt retention due to aldosterone)
□ Growth inhibition if occurs before puberty

Clinical signs:

  • Obesity (lemon on tooth-picks)
  • Moon face
  • Weakness
  • Bruising
  • Acne
  • Striae (thick purple stretch marks around abdomen)
  • Hirtuism in females
  • Menstrual disorders
  • Poor wound healing
  • osteopenia
  • depression and cognitive disorders
91
Q

What is
Androgenital syndrome?

  • what causes it?
  • what does it result in clinically?
  • treatment
A

A group of disorders caused by adrenocortical hyperplasia (enzyme deficit) or malignant tumors, resulting in abnormal secretion of adrenocortical hormones and characterized by masculinisation all but adult men.

-Treat w glucocorticoids

92
Q

Presentation of Congenital adrenal hyperplasia in females vs males

A

Females:

  • infant with ambiguous genitalia at birth
  • premature public hair and enlarged clitoris pre-puberty
  • hirtuism and acne (post-puberty)

Males

  • Adrenal crisis in babies aged 2-3 weeks (salt wasting crisis due to decr aldosterone)
  • premature sexual development (2-3 years old)
93
Q

What is congenital adrenal hyperplasia and what is the most common cause?

A

□ Autosomal recessive mutation caused by the deletion of any of the enzymes involved in cortisol or aldosterone synthesis

□ Leads to decr cortisol and aldosterone and EXCESS androgen (one pathway is blocked, the other is over-stimulated)

□ 21 beta hydroxylase the most common deletion

94
Q

What is the disease state of the adrenal medulla?

What are SX
How do you diagnose it and what is the treatment?

A

Pheochromocytoma:

  • SX are PAROXYSMAL (attacks lasting <1hour): pallor malignant HTN, palpitations, arrhythmias, headaches, sweating, anxiety
  • Diagnosis: serum and 24 hour urinary catecholamine levels; CT

-Treatment: surgical removal
preceded by alpha adrenergic blockade and beta blockers

95
Q

Multiple endocrine neoplasia syndromes:

MEN1 vs 2

what is the mode of inheritance?

A

Multiple endocrine neoplasia involves tumors in AT LEAST 2 endocrine glands

Autosomal dominant

MEN1:
Tumours of
- Pituitary (prolactinoma, GH, ACTH, non-hormone secreting)
- Pancreas (insulinoma, gastrinoma)
- Parathyroid

MEN2:

  • Medullary carcinoma of thyroid (>90%)
  • Pheochromocytoma (40-50%)
  • Parathyroid hyperplasia (10-20%)
96
Q

Clinical effects due to pituitary tumours

A

Upper extension: Upper outer visual field quadrant loss

Downwards extension through sphenoid bone into sinus: CSF rhinorrhoea

Lat extension: CN palsies and temporal lobe epilepsy

Headaches due to stretching of dura and hydrocephalus

97
Q

Types of pituitary adenoma

WHICH IS MOST COMMON?

A

Classified by hormone secreted

  • Prolactinoma (most common)
  • Cortisol secreting
  • GH secreting
98
Q

SX of prolactinoma in men and women.

What is the treatment?

A

Excess prolactin secreted from pituitary tumour

SX women: Hypogonadism (infertility, amenorrhoea or oligomenorrhea) and Galactorrhea

SX men: hypogonadism ( gynaecomastic, decr libido, impotence and infertility); rarely galactorrhea

TX: DA agonist (because DA tonically inhibits production of prolactin)

99
Q

Investigating Cushing’s

A

UEC (hypokalaemia), BSL
24 hour urinary cortisol
Overnight dexamethasone suppression test (fails to suppress cortisol)
CT of adrenals and pituitary

100
Q

Clinical features of acromegaly

A

Enlarged jaw, hands, feet
Coarsening of facial features, enlarged frontal bones and nose
Enlarged tongue and thickened skin and lips

Deeper, louder voide (widened larynx)

Carpal tunnel syndrome (thickened connective tissue)

Enlarged viscera

Early OA

Multi nodular goitre

101
Q

Investigating acromegaly

A

Serum GH and IGF-1 are increased

OGTT suppression test (fails to suppress GH)

CT/MRI of pituitary

102
Q

Treatment of pituitary tumours

A

Transphenoidal hypophysectomy to remove tumour

103
Q

medical options to treat acromegaly

A

Octreotide (somatostatin analogue which suppresses GH and IGF secretion)

Bromocriptine (DA agonist, suppresses GH secretion)

104
Q

What is conn’s syndrome?

Common causes

Clinical triad

A

Primary hyper-aldosteronism

Causes

  • Adrenal adenoma producing aldost.
  • Idiopathic hyperaldosteronism
  • Adrenal carcinoma producing aldost.

Clinical triad

  1. HTN and hypernatraemia
  2. Hypokalaemia (weakness, cramping, bradycardia)
  3. Metabolic alkalosis (Lose K AND H+ to offset Na retention)
105
Q

Investigations and treatment for Conn’s syndrome

A
  1. 24 hour urine - K wasting
  2. Plasma renin (decr) and aldosterone (incr)
    - > high Aldosterone: Renin ratio
  3. CT or MRI of adrenals

Treatment

  • Surgical removal
  • Aldactone (aldosterone antagonist)
  • Amiloride (blocks Na channels in proximal tubule and spares K)
106
Q

BMIClassifications

A

18.5-24.9 normal
25-29.9 overweight
30-39.9 obese
40+ morbidly obese

107
Q

Causes of secondary obesity

A

Endocrine

  • Hypothyroid
  • Cushing’s
  • Insulinoma
  • Hypothalamic
  • PCOS
  • hypogonadism

Medications
- OCP etc

Psychosocial

  • Smoking cessation
  • Eating disorders
108
Q

Causes of hyperparathyroidism

A

Primary

  • PT adenoma (80% cases, benign)
  • PT hyperplasia
  • PT carcinoma
  • MEN I and IIa

Secondary

  • CRF
  • Vitamin D deficiency
  • Other causes low serum Ca
109
Q

Clinical presentation of hyperparathyroidism

A

Primary - 75% asymptomatic
- Sx due to hypercalcacemia non-specific: weakness, fatigue, depression, bone pain, myalgia, LOA, nausea, vomiting, diarrhoea, kidney stones, osteoporosis

Secondary - SX due to ricketts, osteomalacia, renal osteodystrophy

110
Q

Investigations for diagnosis of suspected hyperparathyroidism

A

Serum Ca (high for primary, low/normal for secondary)

Serum PTH (high)
Serum ALP, phosphate

Parathyroid immunoassay

Nuclear medicine - technetium scan

111
Q

Causes of hypoparathyroidism

A

Removal/trauma to gland during surgery

Autoimmune polyendocrine syndromes

Haemochromatosis (iron infiltration and dysfunction)

Mg deficiency

Congenital syndromes

112
Q

Clinical presentation of low serum Ca (hypoparathyroidism amongst causes)

A

Paraesthesia
Muscle cramps and spasm (tetanus)
Fatigue, headaches, bone pain, insomnia
Seizures and arrhythmias

113
Q

5 alpha reductase - what does this enzyme do

A

converts testosterone to DHT

114
Q

aromatase - what does this enzyme do? what does a deficiency in this enzyme mean?

A

Converts testosterone to estradiol

Deficiency in females means androgens circulate at high levels -> masculinisation

115
Q

Clinical presentation of androgen deficiency: onset in adult men

A

General

  • Decr sense of wellbeing, poor concentration, depression, irritability
  • Fatigue, poor stamina
  • Hot flushes, sweats

Sexual

  • Reduced libido
  • Decr erections

Signs

  • Incr fat mass, decr muscle mass
  • Gynaecomastia
  • Osteoporosis
  • Small/shrinking testes
116
Q

Clinical presentation of androgen deficiency when onset in:

  1. 1st trimester
  2. 3rd trimester
  3. Pre-puberty
A
  1. 1st trimester
    - Partial virilisation (masculinisation of fetus)
    - Ambiguous genitalia
    - Complete testosterone deficiency
    - Female external genitalia
  2. 3rd tri
    - Micropenis
    - Crypochordism (no testes)
  3. Pre-puberty
    - Incomplete pubertal maturation
    - Testes <4ml
    - Eunuchoidal body habitus
117
Q

How do you test for aldosterone deficiency?

A

Morning serum total testosterone levels: low if T<10 (repeat to confirm, and do SHBG to rule out falsely low TT)

If low, do LH and FSH
Incr LH, FSH -> primary testicular failure
- acquired (trauma/damage by CTX,RTX,toxins/orchiitis)
- congenital (kleinfelter XXY, do karyotyping to confirm)

Normal/low FSH/LH -> secondary hypogonadism

  • tumour, surgery, trauma, infiltration
  • genetic
  • hyperprolactinaemia,obesity, cushing’s
118
Q

Causes of erectile dysfunction

A

Drugs
- anti HTN, anti depressants, anti-psychotics

Vascular (smoking, metabolic disease)

Nerves S2-4 (shoot) and PS (point) damage via surgery or spinal trauma

Penile damage

Psychological (if they get morning erection, wet dreams, can masturbate etc)

Pituitary - ask about headaches and visual disturbance

119
Q

Interpreting a snellen chart

A

As 6/number by line on chart that they
could read successfully (e.g. 6/5)

if the patient
read line 9 but got 1 letter wrong their acuity would be 6/9-1 (and vise-versa)

MD2 (16 decks)

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