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35 Cards in this Set

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Cushing syndrome

XS cortisol

Cushing causes

Exogenous corticoS - decreased ACTH -> bilateral adrenal atrophy


Adrenal - primary A adenoma, hyperplasia, Ca - decreased ACTH -> atrophy of uninvolved A gland - can PC as primary aldosteronism = Conn syndrome


ACTH secretion - paraneoplastic (small cell lung ca, bronchial carcinoids), ACTH secreting pituitary adenoma = Cushing disease - increased ACTH -> bilateral adrenal hyperplasia

Cushings findings

HT


Weight gain


Moon facies


Truncal obesity


Buffalo hump


Hyperglycaemia - insulin resistance


Skin changes - thinning, striae


Osteoporosis


Amenorrhea


Immune suppression

Cushings dx

Increased free cortisol on 24hr urine analysis


Midnight salivary cortisol


Overnight low-dose dexamethasone suppression test


Low ACTH: Suspect adrenal tumor = ACTH independent Cushing syndrome - MRI to confirm


High ACTH: Distinguish between Cushing disease and ectopic ACTH secretion = high-dose dexoM suppression test and CRH stimulation test


- Ectopic secretion: No suppression after dexoM, no increase with CRH


- Cushing disease: Suppression, increase in ACTH and cortisol

Primary hyperaldosteronism

Adrenal hyperplasia


Conn syndrome = aldosterone secreting adrenal adenoma


=> HT, hypoK, metabolic alkalosis, low plasma renin


Normal Na and no edema due to aldosterone escape mechanism


Uni or bilateral


TX: Surgery to remove tumour +/- spironolactone = K sparing diuretic, aldosterone antagonist

Secondary hyperaldosteronism

Renal perception of low intraV volume -> overactive renin-angiotensin system


Renal A stenosis, CHF, cirrhosis, nephrotic syndrome


High plasma renin


TX: Spironolactone

Addison disease

Chronic primary adrenal insufficiency


Due to renal atrophy or destruction by disease - autoimmune, TB, metastasis


Aldosterone and cortisol deficiency -> hyponatremic volume contraction -> hypotension


HyperK, acidosis, skin and mucosal hyperpigmentation (MSH - by product of XS ACTH production from POMC)


Adrenal atrophy


Absence of hormone production


All 3 cortical divisions - spares medulla


Secondary adrenal insufficiency - decreased pituitary ACTH production - no skin/mucosal hyperpigmentation, no hyperK

Waterhouse-Friderichsen syndrome

Acute primary adrenal insufficiency


Due to adrenal haemorrhage


A/W Neisseria meningitidis septicaemia, DIC, endotoxic shock

Neuroblastoma

Tumour of adrenal medulla


Children - under 4yo


From neural crest cells


Occurs somewhere along sympathetic chain


PC - ab distention, firm irregular mass that can cross the midline


Homovanillic acid HVA - bd product of dopamine - increased in urine


Bombesin +


Less likely to develop HT


A/W overexpression of N-myc oncogene

Pheochromocytoma

Tumour of adrenal medulla


Adults


Derived from chromaffin cells - neural crest


10s - 10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids

PheoC symptoms

Most secrete epiN, NE, dopamine -> episodic HT


A/W von Hippel-Lindau dx, MEN 2A/B


Symptoms in spells - release and remit

5 Ps


Pressure - HT


Pain - headache


Perspiration


Palpitations - tachyC


Pallor

PheoC findings

Urinary VMA = bd product of NE and epiN


Plasma catecholamines increased

PheoC treatment

Irreversible alpha-antagonists - phenoxybenzamine


Beta-blockers


Followed by tumour resection


Alpha-blockade must be achieved before giving beta to avoid hypertensive crisis

Hypothyroidism

Cold intolerance


Weight gain


Decreased appetite


Hypoactivity


Lethargy


Fatigue


Weakness


Constipation


Hyporeflexia


Myxedema - facial, periorbital


Dry cool skin


Coarse brittle hair


BradyC


Dyspnea on exertion


Increased TSH


Decreased free T3/T4


Hypercholesterolemia - low LDL expression

Hyperthyroidism

Heat intolerance


Weight loss


Increased appetite


Hyperactivity


Diarrhoea


Hyperreflexia


Pretibial myxedema - graves dx


Periorbital edema


Warm moist skin


Fine hair


Chest pain


Palpitations


Arrhythmias


Increased no of and sensitivity of beta adrenergic receptors


Decreased TSH


Increased free or total T3/4


Hypocholesterolemia - increased LDL receptor expression

Hashimoto thyroiditis

HypoT


Autoimmune disorder


Antithyroid peroxidase, antithyroglobulin Abs


HLA-DR5


Increased risk of non-Hodgkin lymphoma


Early hyperT - thyrotoxicosis during follicular rupture


Hurthle cells


Lymphoid aggregate + germinal centres


Moderately enlarged nontender thyroid

Congenital hypoT = cretinism

HypoT


Severe, fatal


Due to maternal hypoT, thyroid agenesis, T dysgenesis, iodine def, dyshormonogenic goiter


Pot bellied


Pale


Puffy faced child


Protruding umbilicus


Protrubent tongue


Poor brain development

De Quervain thyroiditis

Subacute hypoT


Self limited, often following flu-like illness


Early hyperT


Granulomatous inflammation


Increased ESR


Jaw pain


Early inflammation


Very tender thyroid


PAIN

Riedel thyroiditis

HypoT


Thyroid replaced by fibrous tissue


Fibrosis may extend - locally - airway - mimicks anaplastic carcinoma


Manifestation of IgG4-related systemic disease


Fixed hard rock like and painless goiter

Other causes of hypoT

Iodine def


Goitrogens


Wolff-Chaikoff effect


Painless thyroiditis

Toxic multinodular goiter

HyperT


Focal patching of hyperfxn follicular cells


Work independently of TSH due to mutation in TSH receptor


Increased release of T3/4


Jod-Basedow phenomenon: Thyrotoxicosis if pt with iodine def goiter is made iodine replete

Graves' disease

HyperT


AutoAb IgG stimulate TSH receptors on thyroid


Diffuse goiter


Retro-orbital fibroblasts - exophthalmos: proptosis, extraocular muscle swelling


Dermal fibroblasts - pretibial myxedema


Often presents during stress - childbirth

Thyroid storm

HyperT


Stress-induced catecholamine surge


Complication of graves and other hyperT disorders


PC: Agitation, delirium, fever, diarrhoea, coma, tachyA -> death


Increased ALP due to increased bone turnover


TX = 3Ps - propranolol, Propylthiouracil, prednisolone

Thyroid cancer

Thyroidectomy


Surgery - hoarseness, hypoCa, transection of inf thyroid A

Papillary ca

Most common


Excellent prognosis


Empty appearing nuclei = Orphan Annie eyes


Psammona bodies


Nuclear grooves


Increased risk with RET and BRAF mutations, childhood irradiation

Follicular ca

Good prognosis


Invades thyroid capsule


Uniform follicles

Medullary ca

From Parafollicular C cells


Produces calcitonin


Sheets of cells in amyloid stroma


A/W MEN 2A/B - RET mutations

Anaplastic ca

Undifferentiated


Older pts


Invades local structures


Very poor prognosis

Lymphoma

A/W Hashimoto thyroiditis

Primary hyperParaT

Adenoma


HyperCa


HyperCalciuria


HypoPhosphatemia


Increased PTH


Increased ALP


Increased cAMP in urine


Asymptomatic


PC: Groans, stones, moans, bones


Osteitis fibrosa cystica = cystic bone spaces filled with brown fibrous tissue - bone pain

Secondary hyperParaT

Due to decreased gut Ca absorption and increased PO4


Chronic renal disease - hypoVitD -> deceased Ca absorption


HypoCa


HyperPhosphatemia - in chronic renal failure, hypo in other causes


Increased ALP


Increased PTH


Renal osteodystrophy: Bone lesions due to renal dx

Tertiary hyperParaT

Refractory hyperPT from chronic renal disease


Increased PTH


Increased Ca

HypoParaT

Accidental surgical excision of paraT glands, autoimmune destruction, DiGeorge syndrome


HypoCa


Tetany


Chvostek sign - tapping of facial nerve -> contraction of facial muscles


Trousseau sign - occlusion of brachial A with BP cuff -> carpal spasm

PseudohypoParaT

= Albright hereditary osteodystrophy


AD


Unresponsiveness of kidney to PTH


HypoCa


Shortened 4th/5th digits


Short stature

Pituitary adenoma

Prolactinoma - most common


Functional - hormone producing - PC based on hormone produced


Non functional - silent - PC with mass effect - bitemporal hemianopia, hypopituitarism, headache


PL - amenorrhea, galactorrhea, low libido, infertility - TX: dopamine agonists - bromocriptine