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FINALS > ENDOCRINOLOGY > Flashcards

ENDOCRINOLOGY Flashcards

1
Q

What does PTH do?

A

Increases serum calcium

Increases osteoclast activity to increase bone turnover releasing calcium and phosphaye

Increasesvitamin D3 production

Increases uptake of calcium in the kidneys

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2
Q

What are the causes of Primary Hyperparathyroidism?

A

Cancer of the parathyroid gland
80% Solitary Adenoma

(multifocal disease, hyperplasia, multiple adenoma, parathyroid carcinoma)

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3
Q

What are the clinical features of Primary Hyperparathyroidism?

A
  • Elderly females with unquenchable thirst with inappropriately normal or raised parathyroid hormone*

Signs of hypercalcaemia

HTN
Raised ALP

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4
Q

How is Primary Hyperparathyroidism managed?

A

Fluids prevents stones

Total parathyroidectomy (remove the parathyroid glands) if:

  • High blood calcium: Serum Calcium >1mg/dL above noral
  • High urine calcium: Hypercalciuria >400 mg/day
  • Life threatiening hypercalcaemia
  • Nephrolithiasis
  • > 50 y/o
  • Neuromuscualr symptoms
  • Reduction in bone mineral density

Calcimimetic agents: cinacalcet if not suitable for surgery

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5
Q

What causes Secondary Hyperparathyroidism?

A

Parathyroid gland HYPERPLASIA due to LOW CALCIUM due to CKD

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6
Q

What are the clinical features of Secondary Hyperparathyroidism?

A

Few symptoms

Eventually bone disease
Soft tissue calcification

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7
Q

How is Secondary Hyperparathyroidism managed?

A

Manage medically, indications for parathyroidectomy:

  • Bone pain
  • Persistent pruritis
  • Soft tissue calcification
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8
Q

What are the causes of Tertiary Hyperparathyroidism?

A

Ongoing hyperplasia of all 4 glands after CKD is corrected

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9
Q

What are the clinical features of Tertiary Hyperparathyroidism?

A 
Metastatic calcification
Bone pain and/or fractures
Nephrolithiasis
Pancreatitis
Raised ALP
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10
Q

How is Tertiary Hyperthyroidism managed?

A

Only treat after 12 month persistance because it usually resolves

Remove culprit gland or all

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11
Q

What are the causes of Malignant Hyperparathyroidism?

A

PTH related-peptide produced by some Squamous cell Lung cancers, Breast cancers and renal cell carcinomas

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12
Q

What are the hormone levels in the hypeparathyroidisms?

A

1’ Raised: PTH Calcium
Low: Phosphate

2’ Raised: PTH Phosphate
Lowered: Calcium Vitamin D

3’ Raised: PTH Calcium
Lowered: Phosphate Vitmain D

Malignant: Raised: Calcium
Lowered: PTH (because PTHrp is raised)

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13
Q

What are the causes of primary hypoparathyroidism?

A

Gland failure

  • AI
  • Di geoge syndrome
  • Thyroid surgery
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14
Q

What are the features of primary hypoparathyroidism?

A

Hypocalcaemia

High phosphate

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15
Q

How is primary hypoparathyroidism manged?

A

Calcium supplements
Calcitriol
Synthetic pTH

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16
Q

What are the causes of secondary hypoparathyroidism?

A

Radiaiton
Surgery
Hypomagensia

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17
Q

What is pseudo hypoparathyroidism?

A

Target cells are insensitive to PTH (due to a G protein abnormality) so PTH is actually high (calcium is low)

  • Low IQ
  • Short stature
  • Short 4th abd 5th metacarpals
  • Calcified basal ganglia
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18
Q

What is pseudopsuedo hypoparathyroidism?

A

Same features but normal biochemistry

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19
Q

What do the zones of the Adrenal Cortex produce?

A

Zona Glomerulosa- Mineralcorticoids
Zona Fasiculata- Glucocorticoids
Zona Reticularis- Sex steroids

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20
Q

What is Cushing’s syndrome?

A

CLINICAL STATE reduced by chronic EXCESS of GLUCOCORTICOIDS, loss of normal feedback mechanism and loss of CORTISOL secretion circadian rhythm

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21
Q

What are the causes of Cushing’s syndrome?

A

ACTH independent:
the adrenal gland is making too much cortisol and the ACTH is low. ADRENAL TUMOUR or bilateral adrenal hyperplasia

ACTH dependent:

  • Cushing’s disease: Bilateral adrenal hyperplasia from PITUITARY ADENOMA secreting ACTH
  • ECTOPIC ACTH production e.g. Small cell lung cancer
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22
Q

What are the symptoms of Cushing’s syndrome?

A

Acne
Mood changes (depressed, lethargic irritable, psychosis)
Hirsutism
Increased weight
Acanthiosis Nigricans (brown velvety skin discoloration e.g. in axilla)
Erectile dysfunction/Irregular menses
Recurrent achilles tendon rupture

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23
Q

What are the signs of Cushing’s syndrome?

A 
Infections
Moon face
Buffalo hump
Central obesity
Purple striae 
Poor healing
Skin and muscle hypertrophy
Bruising
Osteoporosis
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24
Q

What are the tests for Cushing’s syndrome?

A

1st line:
- overnight DEXAMETHASONE SUPRESSION TEST (should suppress to <50nmmol/L
or
- 24 hour urinary free cortisol

2nd line:
48 hour dexamethasone suppression

High-dose DMST differentiates between pituitary and non-pituitary causes

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25
Q

What is Primary Adrenal Insufficiency?

A

Autoimmune (Addison’s), Infective (TB, HIV, meningiococcal septicaemia), Metastases and Anti-phospholipid syndrome cause significant BILATERAL damage to the adrenal glands. This IMPAIRS ALL 3 LAYERS of the cortex and loss of negative fb causes the PITUITARY INCREASES ACTH PRODUCTION

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26
Q

What are the signs and symptoms of reduced function of the Zona Glomerulosa?

A

Reduced production of mineralcorticoids so reduced serum aldosterone.

Increased sodium lost -> HYPONATRAEMIA -> water lost -> HoTN (postural)-craving for salt
K+ retained -> HYPERKALAEMIA
H+ retained -> METABOLIC ACIDOSIS

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27
Q

What are the signs and symptoms of reduced function of the Zona Fasiculata?

A

Reduced production of glucocorticoids so reduced serum cortisol

Reduced ability to mobilise glucose into blood stream causes HYPOGLYCAEMIA

Increased Vasodilation (cortisol is a vasoconstrictor) HOTN (POSTURAL)

SIADH (cortisol usually inhibits) HYPONATRAEMIA

MALAISE
FATIGUE
ANOREXIA
WEIGHT LOSS
WEAKNESS
ABDOMINAL PAIN
JOINT AND MUSCLE PAIN
N&amp;V
MOOD CHANGES: depression and psychosis
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28
Q

What are the signs and symptoms of reduced function of the Zona Fasiculata?

A

Reduced testosterone in women (because adrenals are only source)

Reduced axillary and pubic hair, reduced libido

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29
Q

How is Primary Adrenal Insufficiency tested for?

A

Raised ACTH from pituitary due to lack of negative feedback from cortisol.

Short SYNACTHEN test: measure cortisol 30 min before and after giving 250ug IM of synacthen

9am cortsol <500mmol/L

Serum aldosterone levels

Na+, K+, BM, pH

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30
Q

How is Primary Adrenal Insufficiency managed?

A

Give HYDROCORTISONE
20-30mg/day in 2-3 divided doses with the majority in the morning
Avoid late in the day-can cause insomnia
Don’t stop
Double the dose if infection or increased stress

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31
Q

What is Acromegaly?

A

Excess of growth hormone

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32
Q

What are the causes of Acromegaly?

A

95% due to PITUITARY ADENOMA

<5% due to ectopic GHRH or GH production by other tumours

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33
Q

What are the features of Acromegaly?

A

Enlarged features, organs and

  • Headaches
  • Supraorbital bulging
  • Vision defects
  • Enlarged lips, tongue and nose: coarse features
  • Jaw and dental changes
  • Thyroid hypertrophy
  • Voice changes
  • Skin tags
  • Galactorrhoea due to prolactin increase
  • Cardiomegaly
  • Hepatospleonmegaly
  • HTN
  • Carpal tunnel and enlarged hand breadth and feet
  • Bowel polyps
  • Nephromegaly
  • Enlarged colon
  • Acanthinosis Nigricans
  • Osteoarthritis
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34
Q

What are the complications of Acromegaly?

A

HTN
DMT2
Cardiomyopathy
Colorectal cancer

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35
Q

How is Acromegaly tested for?

A

GH is not diagnostic

  • OGTT with serial GH measurements, hyperglycaemia usually suppresses
  • 25% have impaired glucose tolerence
  • IGF-1 will be high
  • MRI will show a pituitary tumour
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36
Q

How is Acromegaly managed?

A

Trans sphenoidal surgery to remove pituitary tumour

Somatostatin analouge inhibits GH

External irradiotion

Dopamine agonists used for raised prolactin

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37
Q

What is Metabolic Syndrome?

A

3 or more of:

  • High waist circumference
  • BMI >30 (central obesity)
  • Raised trigylcerides
  • Low HDL
  • HTN
  • Raised fasting blood glucose

individuals have insulin resistance (in muscle, liver and adipose) resulting in high levels of circulating insulin and C-Peptide levels

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38
Q

What is a phaeochromocytoma?

A

Neuroendocrine tumour of cromaffin cells in medulla of the adrenal glands that secretes high amounts of CATECHOLAMINES (mostly Noradrenaline and some Adrenaline)

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39
Q

How do Phaeochromocytomas present?

A

Sympathetic nervous system hyperactivity

  • Skin sensations
  • Riased H.R and Palpitations
  • Raised BP
  • Anxiety
  • Diaphoresis (sweating)
  • Headaches
  • Pallor
  • Weight loss
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40
Q

How are Phaeochromocytomas managed?

A

Measure catecholamines and metanephrines in blood
or urine

Give alpha adrenoceptor blocker (e.g. phenoxybenzamine) or SAA Antagoinst to preduce risk of hypertension during surgery

Salt load due to volume depletion

NEVER USE NON-SELECTIVE B BLOCKERS

Syrgically resect

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41
Q

What is the inheritence pattern of Multiple Endocrine Neoplasias?

A

A.D

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42
Q

What is MEN-I?

A

3 Ps

Parathyroid: hyperplasia -> hyperparathyroid

Pituitary tumours e.g. Prolactinoma

Pancreatic tumours e.g insulinoma/glucagonoma

+ adrenal
+ thyroid

MEN-I gene

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43
Q

What is MEN-IIa?

A

2 Ps

Medullary THYROID CA

Paraythyroid
Pheochromocytoma

RET Oncogene

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44
Q

What is MEN-IIb?

A

1 P

Medullary THYROID CA

Pheochromocytoma

+ marfanoid
+neuromas-thickening of nerve tissue in parts of body

RET Oncogene

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45
Q

What is Diabetes Mellitus?

A

Chronic hyperglycaemia due to reduced endogenous insulin or reduced effectiveness of insulin

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46
Q

What is DMT1?

A

AI destruction of B cells in Islets of Langerhans resulting in absolute insulin deficiency

HLA-DR3/4

Presents with: Polyuria, Polydipsia and DKA

47
Q

What is DMT2?

A

Excess adipose tissue results in a RELATIVE INSULIN DEFICIENCY (not enough to go round)

Often found incidentally but may present with polydipsia and plyuria

48
Q

What is Pre-diabetes?

A

FBG: 6.1-6.8

HbA1c : 42-47 (6-6.4%)

Not yet diabetic but likely to go on to develop DMT2 without intervention

49
Q

What is MODY?

A

Maturity Onset Diabetes of the Young

A.R inheritance, affects insulin production

Presents like DMT2 <25y

Sulfonylureas work very well

50
Q

What is LADA?

A

Latent AI Diabetes in Adults

DMT1 that presents later in life

51
Q

What are other causes of Diabetes?

A
  • Acromegaly
  • Chronic pancreatitis
  • Hyperthyroidism
  • Haemochromatosis
  • Phaeochromocytoma
  • Insulinoma
  • Cushing’s (increased glucocorticoids)
52
Q

What are the tests for Diabetes?

A

Finger-prick

One off BG: fasting or non-fasting

HbA1c: average blood sugars over 3 months

GTT: 75mg test blood sugars 2 hours later

53
Q

What are the criteria for diagnosing Diabetes?

A

Symptomatic: Fasting > 7.0 mmol/L
Random (or GTT) >11.1 mmol/L

If Asymptomatic these need to be demonstrated on two separate occasions

HbA1c > 48 (6.5%)

54
Q

When can HbA1c not be used?

A
  • glucocorticoids
  • children
  • haemolytic anaemia
  • untreated iron deficiency anaemia
  • HIV
  • CKD
55
Q

What are the risk factors of Diabetes?

A

Microvascular:

  • Retinopathy
  • Neuropathy
  • Nephropathy

Macrovascular:

  • Stroke (x2)
  • CVD (x4)
56
Q

What blood pressure should be aimed for in Diabetes?

A

<140/80 unless end-organ failure then <135/80

57
Q

What are the stages of Diabetic Retinopathy?

A

Background
Pre-proliferative
Proliferative
Maculopathy

58
Q

What are the features of Background Diabetic Retinopathy?

A
  • Microaneurysms (dots)
  • Haemorrhages (blots)
  • Hard exudates (lipid deposits)

Refer if any of these are near the macula

59
Q

What are the features of Pre-proliferative Diabetic Retinopathy?

A
  • Haemorrhage
  • Venous beading
  • Cotton-wool spots (infarcts)

Refer

60
Q

What are the features of Proliferative Diabetic Retinopathy?

A

New vessels have formed

Refer as an emergency

61
Q

What are the features of Maculopathy Diabetic Retinopathy?

A

Reduced acuity

Due to high retinal blood flow 
Cotton wool spots 
Blot haemorrhages
New vessels 
Ischaemic areas proliferate, bleed, fibrose and detach from the retina

Give prompt steroids

62
Q

What are the types of cataracts?

A

Snowflake-juvenile

Senile- earlier onset in diabetics

63
Q

What are the two types of Diabetic Foot?

A

Ischaemic (micro and macrovascular)

Neuropathic

64
Q

What are the features of Ischaemic Diabetic Foot?

A 
Critical toes
Absent dorsalis pedis -> do doppler
Ulceration
- Punched out
- Painless
- Areas of thick caluss

Check feet, chriopody

65
Q

What are the features of Neuropathic Diabetic Foot?

A

Injury/infection over pressure points e.g. metatarsal heads

Reduced sensation: ‘stocking’ distribution
Test with Monofilament-patchy loss

Absent ankle jerk

Deformities:

  • Pes Cavus: high arch
  • Claw toes
  • Loss of transverse arch
  • Rocker bottom foot
  • Charcot’s foot: repeated joint injury, weakining of the bones
66
Q

How are Diabetic foot problems assessed?

A
  1. Neuropathy: Monofilament
  2. Ischaemia: doppler
  3. Boney deformities: do x-ray
  4. Infection
67
Q

What are the types of Diabetic neuropathy?

A

Symmetrical sensory Polyneuropathy: peripheries ‘glove and stocking’, worse at night

Amyotrophy: painful wastage of Quadriceps of Femoral muscles

Mononeuritis Multiples: damage to >2 nerve arease.g. CN III and VI

Autonomic neuropathy:

  • Postural fall in BP
  • Vagal neuropathy
  • Gastroparesis
  • Gustatory sweating
  • Urine retention
  • Erectile dysfunction
  • Diarrhoea
68
Q

What is Hypoglycaemia?

A

Plasma glucose <3 mmol/L

69
Q

How does Hypoglycaemia present?

A

Autonomic:

  • Dizziness
  • Anxiety
  • Palpitations
  • Tremor
  • Sweating
  • Abdominal pain

Neuroglycopenic:

  • Confusion
  • Coma
  • Seizures
  • Personality changes
  • Mutism
  • Vision issues
70
Q

What are the two types of Hypoglycaemia?

A

Fasting: often in pre-existing diabetes due to INSULIN or SULPHONYLUREAS w/ increased activity, missed meal or overdose

OR

EXPLAIN

EXogenous drugs e.g. access to someone else's diabetic meds
Pituitary insifficiency 
Liver issues
Addison's
Insulinoma/Immune
Non-pancreatic cancer

Post-prandial: e.g. in gastric/bariatric surgery

71
Q

How is Hypoglycaemia managed?

A

ORAL SUGAR + LONG ACTING STARCH

OR

IV 50% Glucose 25-50ml with 0.9% saline

OR

IM Glucagon Img, repeat in 20 min + ORAL CARB

72
Q

What are the causes of Hypothyroidism?

A

Primary: problem with the gland e.g. AI

  • Hashimoto’s
  • Priamry Atrophic Hypothyroidism
  • Subacute Thyroiditis (De Quervain’s)
  • Riedel Thyroiditis
  • Drugs
  • Iodine deficiency (lacking in diet, MCC in developing world)
  • Thyroidectomy or Radioiodine treatment
  • Post-partum

Secondary: pituitary gland disorder e.g. Pituitary Apoplexy

Congenital: Thyroid dysgenesis or dyshomogenesis

73
Q

What are the Congenital Hypothyroidisms?

A

Thyroid Dysgenesis

Thyroid Dyshomogenesis

  • Turner’s
  • Down’s
  • coeliacs

1/4000- Screen at birth with heel-prick and treat within 4 weeks to avoid irreversible cognitive impairment (Cretinism)

Features:

  • Prolonged neonatal jaundice
  • Delayed mental and physical development (short stature)
  • Puffy face
  • Macroglossia
  • Hypotonia
74
Q

What is Hashimoto’s Thyroiditis?

A
  • AI associated with DMT1, Addison’s and Pernicious Anaemia
  • Antithyroglobulin antibodies
  • Antithyroid peroxidase

Can cause transient Thyrotoxicosis in acute phase (Hashitoxicosis)

Firm and Non-tender GOITRE due to LYMPHOCYTIC and PLASMA CELL INFLITRATION

More commen in women, 60-70

75
Q

What is Primary Atrophic Hypothyroidism?

A

Diffuse LYMPHOCYTIC INFILTRATION causing ATROPHY so no goitre

76
Q

What is Subacute Thyroiditis (De Quervain’s) when Hypothyroid?

A

Hypothyroidism 3 weeks after initial onset (prior to this hyper/euthyroid) ultimately caused by viral infection
Painful goitre
Reduced Iodine scan uptake
Increased ESR

77
Q

What is Riedel’s Thyroiditis?

A

Rare

Associated with Retroperitoneal fibrosis

Fibrous tissue replaces the parenchyma causing a HARD and FIXED PAINLESS GOITRE

78
Q

What drugs can cause Hypothyroidism?

A

Lithium

Amiodarone

(Carbimazole)

79
Q

What are the features of Hypothyroidism?

A
  • Dry scalo
  • TATT
  • Dementia
  • Non-pitting oedema
  • Cold intolerence
  • Hoarse voice
  • Bradycardia
  • Weight gain
  • Dry, yellow skin
  • Constipation
  • Carpal tunnel
  • Menorrhagia
  • Myalgia, cramps and weakness
  • Reduced tendon reflexes
  • MACROCYTIC NORMOBLASTIC ANAEMIA
  • Acanthinosis nigricans
80
Q

How is Hypothyroidism managed?

A

Give LEVOTHYROXINE 50-100mg OD

(Start lower in elderly and IHD)

Check levels 8-12 weeks after dose change
INCREASE by 25-50mg in PREGNANCY

81
Q

What are the ARDs of Levothyroxine?

A
  • HYPERTHYROIDISM
  • Reduced BONE MINERAL DENSITY
  • Worsen ANGINA
  • AF
  • Interacts with IRON ABSORPTION so take 2 HOURS apart
82
Q

What are the causes of Thyrotoxicosis?

A

Vast majority is Primary

  • Grave’s disease
  • Toxic Multinodular goitre
  • Drugs
  • Subacute thyroiditis
  • Post-partum thyroiditis in the acute phase
  • Acute phase of Hashimoto’s

Never congenital and only 1% are secondary

83
Q

What is Grave’s disease?

A

50% of Thyrotoxicosis

TSH receptor stimulating antibodies in 90%
Anti-thyroid peroxidase in 75%

Specific signs to Grave's disease:
- EYE involvement
- Pretibial MYXODEMA
- Thyroid ACROPACHY: soft tissue swelling of hands and clubbing
Periositis in metacarpals

Females 30-50

84
Q

What is a Toxic Multinodular Goitre?

A

AUTONOMOUSLY FUNCTIONING thyroid NODULES that secrete excess thyroid hormones

NUCLEAR SCINTIGRAPHY-patchy uptake of iodine

85
Q

What are the drug causes of Thyroiditis?

A

Amiodarone

Levothyroxine

86
Q

What is Subacute Thyroiditis (De Quervain’s)?

A

Following VIRAL Infection

4 PHASES:

1-Acute phase-3-6weeks-HYPERTHYROID

  • Painful goitre
  • Give NSAIDs and steroids

2-1-3weeks-EUTHYROID

3-weeks-months-HYPOTHYROID

4-Structure and function back to normal

Global reduction in thyroid uptake on iodine-131 scan

87
Q

What are the features of Thyrotoxicosis?

A
  • Restless
  • Anxiety (labile emotions)
  • Heat Intolerence
  • Sweating
  • Goitre with nodules and bruit
  • Palpitations, arrhythmias (AF)
  • Palmar Erythema
  • Tremor
  • Diarrhoea
  • Acropachy
  • Oligomenorrhoea
  • Weight loss (although weight gain in 10% of cases)
  • Pretibial Nyoxdena-oedematous swelling above lateral malleoli
  • RAISED ESR, LFT and CA2+
88
Q

How is Thyrotoxicosis managed?

A
  • Thyroidectomy
  • Propanolol
  • Carbimazole 40mg (blocks thyroid peroxidase from coupling and iodinating tyrosine residues on thyrogloblin reducing Thyroid hormone reduced T3 and T4)
    Give in high doses for 6 weeks until Euthyroid
  • Radioiodine
89
Q

What are the ADRs of Carbimazole?

A

Agranulocytosis

Crosses placenta

90
Q

What are the hormone levels in Thyrotoxicosis?

A

TSH down

T4 up

91
Q

What are the hormone levels in Primary Hypothyroidism?

A

TSH up

T4 down

92
Q

What are the hormone levels in Secondary Hypothyroidism?

A

TSH down

T4 down

93
Q

What are the hormone levels in Sick Euthyroidism?

A

TSH down (or normal)

T4 down
T3 down
Caused by a non-thyroidal SYSTEMIC ILLNESS, reversible
TENDER GOITRE

94
Q

What are the hormone levels in Subclinical Hypothyroidism?

A

TSH up

T4 normal

Pre-hypo, T4 still normal
2-5% progression risk/year which is higher if autoantibodies are present

95
Q

What are the hormone levels in Poor Thyroxine Compliance?

A

TSH up

T4 Normal

Patients taking Levothyroxine just before their blood test

96
Q

What are the hormone levels in Steroid use?

A

TSH down
T4 normal

TSH lags

97
Q

How should Sub-Clinical Hypothyroidism be managed?

A

TSH 4-10mU/L + normal T4

IF <65year + symptoms
Trial Levothyroxine (stop if no improvement to symptoms)

IF >80years/asymptomatic
Observe and repeat thyroid function in 6months

TSH >10mU/L
<70years TREAT
>80 Observe and repeat thyroid function in 6months

98
Q

What are the Thyroid Eye Features?

A

Retro-orbital inflammation

No signs, no symptoms
Only signs, no symptoms
Soft-tissue involvement
Ptosis
Exopthalmos
Conjunctival ulceration
Sight-loss
99
Q

What are the types of Thyroid Cancer?

A

Rarely secrete hormones so don’t present with hypo/hyperthyroidisms

PAPILLARY CARCINOMA 70%
FOLLICULAR 20%
MEDULLARY CARCINOMA 5%
ANAPLASTIC CARCINOMA 1%
LYMPHOMA
100
Q

What are the features of Papillary Thyroid Carcinoma?

A

Young females
Very good prognosis

Mix of PAPILLARY and COLLOIDAL filled follicles
Tumour papillary projections + pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominately to cervical lymph nodes

Thyroglobulin tumour marker

101
Q

What are the features of Follicular Thyroid Cancer?

A

ADENOMA: Solitary thyroid nodule (usually) can be toxic and produce T3 + T4

CARCINOMA: females >50

  • Macroscopically encapsulated, microscopically capsular invasion can be seen
  • Vascular invasion predominates
  • Multifocal disease is rare

Can only tell the diff in hemithyroidectomy
Thyroglobulin tumour marker

102
Q

How are Papillary and Follicular Thyroid cancers?

A
  • Total thyroidectomy
  • Radiodine 131 to kill residual cells
  • Repeat thyroglobulin levels to detect recurrence early
103
Q

What are the features of Medullary Carcinoma?

A

Cancer of parafollicula cells
MEN-2 or sporadic

Secrete Calcitonin so use as tumour marker

Lymphocytic and haemategenous metastasis

Nodal disease = poor prognosis

May have amyloid deposits

104
Q

What are the features of Anaplastic Thyroid Carcinoma?

A

v rARE
Elderly females
Local invasion common
Resect if poss

105
Q

What are the features of Thyroid Lymphoma?

A

Associated with Hashimoto’s

Present with dysphagia or stridor

106
Q

What are the complications of Thyroid surgery?

A
  • Damage to recurrent laryngeal n.
  • Bleeding into a confined space causing respiratory compromise and laryngeal oedema
  • damage to the thyroid gland causing hypothyroidism
107
Q

What is Diabetes Insipidus?

A

polyuria and polydipsia due to lack of ADH or ADH resistance

108
Q

What are the causes of Diabetes Insipidus?

A

Central: LACK of ADH due to damage to the HYPOTHALAMUS and PITUITARY

Nephrogenic: genetic RESISTANCE of kidneys to ADH

Dipsogenic: abnormal thirst mechanism in the hypothalamus

Gestational

109
Q

What are the osmolalities in Diabetes Insipidus?

A

High plasma osmolality

Low urine osmolality <700mOsm/kg

Opposite of SIADH

110
Q

What are the causes of Hyperaldosteronism?

A

Primary: CONN’S
Uni/Bilateral tumour in the adrenal glands

Secondary:

  • Renal artery stenosis
  • Congestive heart failure
  • Cirrhosis
  • Nephrotic syndrome
111
Q

What are the features of Conn’s Syndrome (primary hyperaldosteronism)?

A

High aldosterone:

Hypernatraemia: HTN

Hyperkalaemia:

  • Cramps
  • Paraesthesia
  • Polyuria
  • Polydipsia

and low H+:
Metabolic Alklalosis

112
Q

What is the pathophysiology of Secondary Hyperaldosteronism?

A

Cirrhosis/Npehrotic syndrome - low albumin - low colloid OSMOTIC PRESSURE - HoTN

OR

Renal artery stenosis/HF

all lead to…

Not enough blood to kidney

Increase Renin

Increase aldosterone
detect in venous sampling

113
Q

How are Primary Hyperaldosteronism and Secondary Hyperaldosteronism differentiated?

A

RENIN:ALDOSTERONE RATIO

114
Q

How is Hyperaldosteronism managed?

A

primary: laproscopic removal of adrenal tumours

Sprionolactone: aldoseterone antagonist

FINALS (13 decks)

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