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Meded Path Lectures > Chem Path 2 > Flashcards

Chem Path 2 Flashcards

1
Q

Roles of T4

A

Regulating basal metabolic rate

Potentiating responses to catecholamines

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2
Q

Hypothyroidism causes

A

AI (most common in UK) -> Primary atrophic with no goitre, Hashimoto’s (goitre and anti-TPO/TG)

Iodine Deficiency (most common worldwide) 
Surgery/radioactive ablation

Drugs

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3
Q

Which drugs can cause hypothyroidism

A

Lithium, Amiodarone, Carbimazole

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4
Q

How does amiodarone affect the thyroid gland?

A

Hyper -> Contains iodine, used as substrate to synthesise thyroxine

Hypo -> Amiodarone is toxic to thyroid tissues

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5
Q

Hypothyroidism Management

A

Levothyroxine orally
Titrate to normal TSH, 6 weekly TSH tests
Higher dose in pregnancy

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6
Q

How to treat myxoedema coma

A

IV Liothyronine

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7
Q

Sick euthyroid

A

In severe illness, body shuts down metabolism to conserve energy

Low T3/4

High TSH then low TSH

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8
Q

Subclinical Hypothyroidism

A

Pre-hypothyroid with pituitary compensation

High TSH, normal T3/4

High chance of hypothyroidism if Anti-TPO positive

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9
Q

Causes of Hyperthyroidism

A 
AI - Graves'
De Quervain's 
Thyroid Adenoma
Amiodarone
Toxic Multinodular Goitre
Postpartum
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10
Q

Graves’ Specific symptoms

A

Pretibial Myxoedema

Grave’s Orbitopathy (Proptosis)

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11
Q

Investigations in Hyperthyroidism

A

ECG
TFTs, U&Es, Anti-TSHr
USS
Thyroid Uptake scan

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12
Q

Hyperthyroidism management

A

Smoking cessatioon

Carbimazole/Propylthiouracil (Titrate or block and replace)
Beta Blockers
Lugol’s Iodine
Radio-iodine

Thyroidectomy, must be euthyroid before surgery

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13
Q

Pituitary Mass

A

Adenoma
Macroadenoma = >1cm, non-functional but can be prolactinoma

Microadenoma =<1cm, secrete GH/Prolactin, cause acromegaly

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14
Q

Pituitary Mass Symptoms

A

Bitemporal Hemianopia

Hyperprolactinaemia = gynaecomastia, galactorrhoea, amenorrhoea, loss of libido, impotence

Somatotrophin = Acromegaly (Tissue growth, heart failure, hypertension, DM)

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15
Q

Investigating Pituitary Mass

A

Imaging

Acromegaly -> IGF-1 > OGTT

Prolactin >6000 = prolactinoma

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16
Q

Pituitary Mass management

A

Octeotride (somatostatin analogue)

Cabergoline/Bromocriptine (Dopamine agonist)

Pegvisomat (GH Receptor Antagonist)

Radiotherapy

Trans-sphenoidal debulking

Monitor with GH/Prolactin

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17
Q

Thyroid Tumours

A

Papillary >

Follicular (Good prognosis) >

5% Medullary (MEN2, C-Cells and calcitonin) >

Lymphoma (risk in Hashimoto’s) >

Anaplastic -> Elderly, undifferentiated, poor prognosis

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18
Q

Treatment of Papillary/Follicular Thyroid Tumour

A

Sugery +/i radioactive iodine

Replace thyroxine to suppress TSH

Monitor Thyroglobulin levels

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19
Q

Which pituitary cells do hypothalamic hormones stimulate

A

DA -/> Lactotroph -> Prolactin

TRH -> Thyrotroph -> TSH

VP/CRH -> Corticotroph -> ACTH

GnRH -> Gonadotrophs -> LH/FSH

GHRH -> Somatotrophs -> GH

SS -/> Somatotrophs

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20
Q

Hypopituitarism causes

A

Malignancy (Adenoma>Craniopharyngioma)

Infection -> TB, syphilis

Infiltrative -> Sarcoid, Lymphoma

Iatrogenic -> Surgical, Trauma, radiation

Infarct -> Sheehan’s, Apoplexy

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21
Q

Hypopituitarism Presentation

A

Generic = Wt gain, tiredness, low bp etc

Sex Hormones = impotence, no periods/libido

ACTH = Addisonian Crisis

TSH = Myxoedema Coma

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22
Q

Hypopituitarism Investigation

A

Combined Pituitary Function Test

Give GnRH, TRH, Insulin

Measure pituitary hormones every 30 mins

CT/MRI

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23
Q

Hypopituitarism Management

A

Replacement cheaper/easier than control

24
Q

Adrenal Histology

A

Outside to Inside

Capsule 
Glomerulosa (Aldosterone) 
Fasciculata (Cortisol)
Reticularis (Sex Hormones)
Medulla (Catecholamines)
25
Q

Addison’s

A

Low Aldosterone and Cortisol

26
Q

Addison’s Causes

A

Primary = Iatrogenic, AI, TB, Infarct, Malignancy

Secondary = Pituitary

27
Q

Addison’s Presentation

A 
Postural Symptoms 
Wt Loss
Fatigue
Vomiting, Salt Craving 
Skin/Mucosal Pigmentation
28
Q

Addison’s Investigations

A

9am Cortisol >350 excludes

Electrolytes (Low sodium, High Potassium)

Serum ACTH

Glucose

SynACTHen rises in secondary disease

29
Q

Addison’s Management

A

Replace w/ Hydro/Fludrocortisone + Sick day rules

30
Q

Cushing’s causes

A

Primary = adrenal malignancy

Secondary = Pituitary adenoma, ectopic production, ACTH (SSLC)

Iatrogenic

31
Q

Cushing’s investigations

A

Dexamethasone Suppression test
Low dose confirms Cushings
High dose determines cushings syndrome or disease

32
Q

Cushing’s Management

A

Primary -> Adrenalectomy +/- steroid replacement

Ectopic -> Ketoconazole, Metyrapone, Mifepristone

33
Q

Nelson’s Syndrome

A

Adrenal removal leads to raised ACTH, causing ACTH producing pituitary tumour to grow

Bitemporal Hemianopia

Tanned

34
Q

Conn’s causes

A

Adrenal Hyperplasia

Adrenal Adenoma/Carcinoma

35
Q

Conn’s Presentation

A

Treatment resistant HTN

Low Potassium
High Sodium

36
Q

Conn’s Investigations

A

Electrolytes, Aldosterone:renin ratio is raised
Adrenal vein sampling
Imaging

37
Q

Conn’s Management

A 
Aldosterone antagonist (Spironolactone)
Surgery
38
Q

Phaeochromocytoma

A

Pulses of HTN, arrhythmias, sweating

Used to be vanillymandelic acid, now 24h catecholamines (TCAs, CCBs, Beta Blockers can cause false positive)

Caused by adrenal medulla tumour (adrenline) or peripheral nerual tumour (noradrenaline)

39
Q

Phaeochromocytoma associations

A

MEN 2 A/B
NF-1
VHL

40
Q

MEN 1

A

Pituitry Adenoma
Parathyroid Hyperplasia
Pancreatic Tumour

41
Q

MEN 2A

A

Phaeochromocytoma
Pituitary Hyperplasia
Medullary Thyroid

42
Q

Men 2B

A

Mucosal Neuroma
Marfinoid
Medullary Thyroid
Phaeochromocytoma

43
Q

T1DM antibodies

A

ICA
IAA
GADA
IA-2A

44
Q

Pre-Diabetes results

A

Fasting - 6.1-6.9
OGTT - 7.8-11
HbA1c - 42-47
Random - 7.8-11

45
Q

Diabetes results

A

Fasting - >7
OGTT - >11.1
HbA1c - >48
Random - >11.1

46
Q

T2DM management

A

Metformin
Add: Sulphonylurea, DPP-4 Agonist, SGLT-2 Inhibitor
Add GLP-1 Agonist or two of above

47
Q

HHS

A

Insulin resistance causes persistent hyperglycaemia
Causes osmotic diuresis

Confusion, dehydration

Raised glucose, osmolarity, usually no ketones/acidosis

48
Q

HHS treatment

A

IV fluids 3-6l/24h
.9%. NaCl +/- KCl

Not too quick as can cause central pontine myelinolysis

Monitor with BMs (fall of 5mM/h) and ketones - add insulin if ketones rising

49
Q

DKA

A

Absolute insulin deficiency
Body starving = unregulated ketosis = acidosis

Causes - common = missed insulin doses

50
Q

DKA investigations

A

ketones >3
pH <7.3
BM>15

Find cause (FBC, cultrues, CXR, Urinalysis)
Find damage (U&Es, ABG, ECG)
51
Q

DKA Management

A

Fluids
Rapid then taper
KCl if <5.5

IV Insulin .1u/kg + normal dose

10% Dextrose when BM<15

Catheter, urine = at least .5ml/kg/hr

Hourly ketones/BM

52
Q

Acute Porphyrias with skin symptoms

A

Variegate Porphyria (Protoporphyrinogen oxidase def.)

Hereditary Coproporphyria ( Copropophyrinogen oxidase def.)

53
Q

Acute Porphyrias

A

Acute Intermittent Porphyria (PBG deaminase/HMB Synthase inhibitor)

ALA-dehydratase deficiency porphyria (ADP)

54
Q

Cutaneous Porphyrias

A

Porphyria cutanea tarda (PCT)

Erythropoietic protoporphyria (EPP)

X-Linked erythropoietic protoporphyria (XLEPP)

Congenital erythropoietic porphyria (CEP)

55
Q

Porphyria?

A

Enzyme deficiency in Glycine/Succinyl-CoA to Haem synthesis pathway leads to buildup of intermediate

Meded Path Lectures (15 decks)

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