Endocrinolgy, Mhu, Mbbs Iv

Front 1

SIADH definition

Back 1

Hyponatremia, inappropriately elevated urine osmolality (>100 mOsm/kg), and decreased serum osmolality in a euvolemic patient. Only in otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function; no diuretics; + other ADH secretion stim, eg. hypotension, severe pain, nausea, and stress.

Has to be in the setting of water intake

Front 2

SIADH, s/s (hyponatraemia)

Back 2

Severe, rapid onset hyponatraemia: Confusion, disorientation, delirium, generalized muscle weakness, myoclonus, tremor, asterixis, hyporeflexia, ataxia, dysarthria, Cheyne-Stokes respiration, pathologic reflexes, generalized seizures, coma.

Slow onset, may have no s/s

Front 3

SIADH, diagnostic criteria

Back 3

Bartter-Schwartz criteria:

- Hyponatremia with corresponding hypo-osmolality

- Continued renal excretion of sodium

- Urine less than maximally dilute

- Absence of clinical evidence of volume depletion

- Absence of other causes of hyponatremia

- Correction of hyponatremia by fluid restriction

Front 4

SIADH, ix

Back 4

- Serum sodium, potassium, chloride, and bicarbonate

- Plasma osmolality

- Serum creatinine

- Blood urea nitrogen

- Blood glucose

- Urine osmolality

- Serum uric acid

- Serum cortisol

- Thyroid-stimulating hormone

Front 5

SIADH/hyponatraemia tx

Back 5

If moderate sympts:

- 3% hypertonic saline (513 mEq/L) + Loop diuretics with saline + Vasopressin-2 receptor antagonists (aquaretics, such as conivaptan) + Water restriction

- If chronic asymptomatic give V2 receptor antags and fluid restrict.

Front 6

SIADH patho

Back 6

non physiological ADH release=>up water reabsorption=>hyponatremia=>volume expansion =>Volume receptors activated +natriuretic peptides secreted=> naturesis and kaliuresis => steady state reached, Na+ excreted = Na intake

Hyponatremia does not occur if water intake is severely restricted.

Front 7

Cerebral complications SIADH

Back 7

Hyponatraemia+hypoosmalality=>acute oedema of brain cells=>cannot expand d/t rigid calvaria=>>5-10% brain water inc.=>cerebral oedma + herniation=>death

dec osmolarity=>brain ECF fluid shift into CSF=>K+ intracellular organic osmolytes lost.

Front 8

Correction Na+ in SIADH

Back 8

Do not correct Na too quickly as risk of central pontine myelenosis.If severe sympts: Correct at max rate 0.5-1 mEq/hr, and not > 10-12 mEq in first 24 hrs. max Na 125-130 mEq/L

Electrolytes rapidly reaccumulate in the brain ECF w/i 24 hours=> overshoot normal conc. Organic osmolytes return v slowly (5-7 days). Electrolytes normal by 5th day after correction, when organic osmolytes return to normal.

Front 9

SIADH aetiology

Back 9

Caused by either inappropriate hypersecretion of ADH from its normal hypothalamic source or by ectopic production. The causes of SIADH can be divided into four broad categories: nervous system disorders, neoplasia, pulmonary diseases, and drug induced (which include those that [1] stimulate AVP release, [2] potentiate effects of AVP action, or [3] have an uncertain mechanism

Millions of things cause it

Front 10

Osteomalacia

Back 10

Failure of osteoid to calcify

Front 11

Rickets

Back 11

Unique to children and adolescents. Failure of osteoid to calcify in a growing person.

Front 12

Cause of rickets

Back 12

Deficiency of Vit D3 (or rarely phosphorus or calcium)

Front 13

Complications rickets

Back 13

- Skeletal deformity and short stature

- In females, pelvic distortion =>childbirth comps - Severe rickets assoc. w resp failure

Front 14

Rickets s/s

Back 14

- Large head and protruding forehead

- Curved humerus, ulna and radius. Femurs and tib/fib with prominent epyphyses at ankle and wrist

- Kyphosis

- Depressed ribs + pectus carinatum

- Protruding abdomen

- Delayed closure anterior fontanelle

- Generalised muscular hypotonia

- Greenstick fractures

Front 15

Rickets patho

Back 15

Vit D-3 defic=> less Ca/phos absorb intest + more phos loss in kid + less direct facilitation of calcification=>hypocalcemia=> inc. PTH=> Inc. renal phosphorus loss=> dec deposition of calcium in the bone.

Front 16

Osteoporosis mgmt

Back 16

- Stop bone damaging meds, adequate exercise, adequate vitamin D (calcitriol) and calc

- Bisphosphonates (alendronate, risendronate)

- SERMs (eg. raloxifen)

- Monitoring (repeat dxa 12-24mnths), referral, injury prevention

Front 17

Metabolic syndrome definition

Back 17

- Low HDL <40mg/dL (m), <50mg/dL (f)

- High central obesity

- High BP >130 syst or >85 diast (or tx for HTN)

- High TAGs >150 mg/dL (or tx for lipid abnorm)

- Elevated fasting glucose >100mg/dL or previously diagnoses DMII

- Need 3/5

Front 18

Glucose transporters

Back 18

GLUT 1 - Blood/brain barrier

GLUT 2 - b Cells during hyperglycaemia, kidney reabsorption of glucose

GLUT 3 - Neurones

GLUT 4 - Insulin dependent, resting skeletal muscle,cardiac muscle, adipose tissue. Ca+ dependent activity (embedding oftransporters into membrane)

Sodium Glucose Transporters (SGLT) - Kidney

Front 19

Insulin independent tissues

Back 19

- Liver

- Brain

- Neurones

- Active skeletal muscle (contraction stimulatesGLUT-4 to be put into memb)

Front 20

Effects of insulin

Back 20

inc .Glucose uptake, inc. Glycogenesis, inc. TAG synthesis, inc. Protein synth, inc. glycolysis

Front 21

Glucagon effects

Back 21

inc. Glycogenolysis, inc. Gluconeogenesis, inc. Lipolysis,

Front 22

Prediabetes definition

Back 22

- Fasting blood glucose 6.1-6.9mmol/L

- Impaired glucose tolerance on OGTT 7.8-11.0mmol/L

- HbA1c: 6.0-6.4%

- 1-5% per yr develop DM

- 50-80% return to normal glucose tol

- Lifestyle mods decrease progression by 58%

Front 23

Secondary causes of DM

Back 23

a. Genetic defects of 􏰁 cell function (e.g. MODY – Maturity-Onset Diabetes of the Young)

or insulin action

b. Diseases of the exocrine pancreas:

• Pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, hemochromatosis

c. Endocrinopathies:

• Acromegaly, Cushing’s syndrome, glucagonoma, pheochromocytoma, hyperthyroidism

d. Drug-induced:

• Glucocorticoids, thyroid hormone, 􏰁-adrenergic agonists, thiazides, phenytoin, clozapine

e. Infections:

• Congenital rubella, CMV, coxsackie

f. Genetic syndromes associated with DM:

• Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome

Front 24

HHS mech

Back 24

Relativelack of/resistance to insulin + physiological stress (infection, acuteillness)=> net further reduction in circulating insulin + inc counterreghormones=>hyperglycaemia + hyperosmolarity=> osmotic diuresis + loss ofelectrolytes=> unknown why they do not develop ketoacidosis.

Contrib facts:

- availability of insulin inamounts sufficient to inhibit ketogenesis but insufficient to preventhyperglycemia.

- Hyperosmolarity may decrease lipolysis,limiting amount FFAs available for ketogenesis. - Levels of counterregulatory hormones lower in patients with HHSthan DKA

- More severe dehydration compared to DKA due to more gradual onset and 􏰄 duration of metabolic decompensation plus impaired fluid intake which is common in bedridden or elderly

• Volume contraction =>renal insufficiency􏰀􏰄=> inc hyperglycemia,􏰄 inc osmolality􏰀=>shift of fluid from neurons to ECF􏰀 =>mental obtundation and coma

Front 25

DKA

Back 25

Glucose can't enter cell b/c no insulin/insulin resistance + no inhibition of B oxidation of FFAs by insulin=>B oxidation FFAs=>acetyl co-A=>forms acidic ketone bodies

Front 26

Metabolicacidosis with high anion gap: CAT MUDPILES

Back 26

Carbon monoxide Alcohol Toluene (paint thinner) Metformin Uraemia DKA Paracetamol/paraldehyde Iron/isoniazid Lactic acidosis Tissue hypoperfusion leads to anaerobic metabolism and increased lactic acid production Aetiology Caused by shock (hypovolaemic, distributive, cardiogenic) Hypoperfusion (carbon monoxide poisoning) Extreme exercise Post grand mal seizure (rare) Type A is hypoxia causing increased lactic acid production Type B enzymes that break down lactic acid aren’t sufficient (toxin induced enzyme failure) Ethylene glycol Salicylates

Front 27

Acidosis with normal anion gap

Back 27

Renal failure Bicarbonate loss Diarrhoea (hyperchloraemic)

Front 28

Hyperthyroidism

Back 28

F:M=5:1

Front 29

HYpothalamus-pituitary-thyroid axis

Back 29

Cold/stress/anxiety => Pulsatile secretion ofThyroid releasing hormone (Hypothalamus)=>Release of thyroid stimulating hormone (Anterior pituitary)=> inc production T3 + T4 (Thyroid)=> negative feedback to ant pitand hypo

Front 30

Causes hypothyroidism

Back 30

· Autoimmune(Hashimoto’s) - autoantibodies against thyroglobulin, TPO, TSH receptor (block)=> dec T3 + T4, inc TSH(primary)

· Pituitarydeficit (adenomas or destruction) (secondary)

· Hypothalamicdeficit (tertiary - rare)

· Peripheralresistance to thyroxine

· Dietaryiodine deficiency

· Hereditaryhormone synth defect

· Defectsin TSH or TRH receptor

· Antithyroiddrugs (eg. Lithium)

· Iatrogenic(treatments for hyperthyroidism)

· Hypothyroid phase of thyroiditis

Front 31

Hyperthyroidism causes

Back 31

· Grave’sdisease

· Toxic multinodular goitre

· Toxic nodule

· Hypersecretingpituitary/hypothalamic tumour· Thyroiditis

Front 32

Complications hypothyroid

Back 32

- Mental retardation (cretinism)

- Child mortality

- Impaired growth and development (esp hearing/speech)

- In pregnancy miscarriage and still birth

- Myxoedema coma

- Pernicious anaemia (Hashimoto’s)

- Depression

Front 33

Hyperthyroidism complications

Back 33

- Osteoporosis ( inc osteoclasticaction)

- AF => thromboembolic complications (eg. Stroke)

- CHF (high output failure - older px)

- Loss of vision

- Pre tibial myxedema => elephantiasis in 5%

- Depression

- Anxiety

Front 34

Grave's disease def

Back 34

- Autoimmune disorder characterized by autoantibodies to the TSH receptor that leads tohyperthyroidism

- association with HLA B8 and DR3

Front 35

Grave's disease patho

Back 35

- Defect in T-suppressor cells

- B lymphocytes produce TSI, binds and stimulates the TSH receptor=>stimulates thyroid

- Can be triggered by postpartum state, iodine excess, lithium therapy, viral/bacterial infections, glucocorticoid withdrawal

- Ophthalmopathy a result of increased tissue volume d/t inflamm+accumulation of glycosaminoglycans, stimulated by TSI=> inc osmotic pressure orbit=> fluid accumulation=>displacement of the eyeball forward

• Dermopathy may be related to cutaneous glycosaminoglycan deposition

Front 36

Toxic multinodular goitre definition and s/s

Back 36

- Autonomous t3/T4 production from a functioning adenoma

- goitre with adenomatous changes

- Tachycardia, HF, arrythmia, sweating, nervousness, tremour, weight loss

- Hyperthyroid precipitated by iodine exposure (eg. contrast medium)

- F>M usually age 50+

Front 37

Thyroid storm

Back 37

- Rare, death rate 10-30%- Sudden exacerbation of all hyperthyroid sx- Often precipitated by infection, trauma, surgery- S/s: extreme hyperthermia, tachycardia/arrythmia/CHF/cardiogenic shock, v/d, vacular collapse, hepatic failure w jaundice, confusion

Front 38

Parathyroid hormone actions

Back 38

· inc tubular reab of Ca++

· inc conversion of 25-Vit D to 1-25 VitD3 (via CYP27B1)

· inc osteoblast differentiation + RANK=> inc boneturnover

· inc Urinary phosphate excretion

· inc gastro Ca++ absorption

- Control by negative feedback of Ca++ levels

Front 39

Mechanism increased calcium in cancer px

Back 39

- 20-30% of px with cancer have hypercalc

- Osteolytic bone lesions=> direct inc inserum Ca++

- PTH related protein released by solid cancers=>inc osteoblasticRANKL + inhibits OPG release=> inc bone resorption=> v much inc. Ca++

- Tumor production of 1,25-dihydroxyvit D(calcitriol).

Front 40

Cushing's syndrome epi

Back 40

- Chief cause is oral steroids.

- Endogenous causes are rare

- 80% are dueto incACTH;

- of these a pituitary adenoma (Cushing’s disease) is the commonest cause

- Peak onset, 30–50yrs, usually microadenoma, F=M

Front 41

Cushing's syndrome caused by ectopic ACTH

Back 41

eg. small cell lung cancer+carcinoid tumours, Specific features: pigmentation (due to v. inc. ACTH), hypokalaemic metabolicalkalosis (v. inc. cortisol leads to mineralocorticoid activity),

- weight loss, hyperglycaemia

- Classical features of Cushing’s are often absent. - Dexamethasone evenin high doses (8mg) fails to suppress cortisol production.

Front 42

ACTH independent causes

Back 42

· Usually due to a hypersecretingadrenal adenoma/carcinoma.

- Rapid onset of symptoms of glucocorticoid XS + hyperandrogenism (from sex hormone production in adrenals) presenting asvirilisation in women or feminisation in men

Front 43

Cushing's syndrome prognosis

Back 43

- Untreated Cushing’s has inc. vascular mortality.

- Treated, prognosis is good(but myopathy, obesity, menstrual irregularity, inc BP, osteoporosis, subtle mood chang-es and DM often remain)

Front 44

1o hyperaldosteronism (Conn's) definition

Back 44

- Excess production of aldosterone, independent of RAAS. => inc. sodium+water retention+decreased renin release.

Consider if the following features: HTN, hypokalaemia or alkalosis insomeone not on diuretics. Sodium tends to be mildly raised or normal.

Front 45

s/s 1o hyperaldosteronism

Back 45

- Often asymptomatic

- Signs of hypokalaemia (fatigue, cramps)

- Weakness (evenquadriparesis)

- Paraesthesiae

- Polyuria

- Polydipsia

- Raised BP (not always)

Front 46

1o hyperaldosteronism aetiology

Back 46

~2⁄3 are due to a solitary aldosterone-producing adenoma (Conn’s syndrome)

~1⁄3 are due to bilateral adrenocortical hyperplasia.

- Rare causes: adrenalcarcinoma or glucocorticoid-remediable aldosteronism (GRA).

Front 47

Glucocorticoid-remediable aldosteronism

Back 47

- In GRA, the ACTH regulatory element of the 11B-hydroxylase gene fuses to the aldosterone synthase gene, increasing aldosterone production, and bringing it under the control of ACTH.

Front 48

Addison's definition

Back 48

- Rare

- Can be fatal

- Destruction of adrenal cortex=>cortisol & aldosterone deficiency

-S/s: very non-specific.

You may diagnose a viralinfection or anorexia nervosa in error (K+ is dec. in the latter but inc. in Addison’s).

Front 49

Addison's aetiology

Back 49

- 80% autoimmune in developed world

- Other causes: TB (commonest cause world wide), adrenal metastases (lung, breast, renal), lymphoma, op-portunistic infections in HIV (eg CMV, Mycobacterium avium, p411); adrenal haem-orrhage

Front 50

s/s addison's

Back 50

- Often diagnosed late: lean, tanned, tired, tearful ± weakness, anorexia,dizzy, faints, flu-like myalgias/arthralgias.

- Mood: depression, psychosis, low self-esteem.12 GI: nausea/vomiting, abdominal pain, diarrhoea/constipation. Think ofAddison’s in all with unexplained abdominal pain or vomiting. Pigmented palmarcreases & buccal mucosa (]incACTH; cross-reacts with melanin receptors). Postural hypo-tension. Vitiligo.

Signs of critical deterioration: Shock (incBP, tachycardia), inc T°, coma.

Front 51

Addison's ix

Back 51

dec. Na+ & inc K+ (d/t dec. mineralocorticoid), dec glucose (due to dec. cortisol).

Also:uraemia, inc Ca2+, eosinophilia, anaemia. - Short ACTH stim test (Synacthen test): Do plasma cortisol before and 1⁄2h after Synacthen. Addison’s is excluded if 30min cortisol >550nmol/L.

NB: in pregnancy and contraceptive pill, cortisol levels maybe reassuring but falsely increased, due to inc. cortisol-binding globulin. Also

•ACTH: 9AM ACTH is inc (>300ng/L: inappropriately high). It is low in secondary causes

•21-Hydroxylase adrenal autoantibodies: +ve in autoimmune disease in >80%

•Plasma renin & aldosterone: To assess mineralocortocoid status.

- AXR/CXR: Anypast TB, eg upper zone fibrosis or adrenal calcification? If no autoantibodies, consider further tests (eg adrenal CT) for TB, histoplasma, or metastatic disease.

Front 52

Definition CKD

Back 52

- Impaired renal function for >3 months based on abnormal structure orfunction, or GFR <60mL/min/1.73m2 for >3 months with or without evidence of kidneydamage.

Front 53

Causes CKD

Back 53

1 Diabetes: 20% UK, 43% USA. Type II >> type I2 Glomerulonephritis: commonly IgA nephropathy, also rarer disorders, eg mesangiocapillary GN, systemic disorders, eg SLE, vasculitis

3 Unknown: up to 20% in the UK have no obvious cause of CKD, many of these present late with small, shrunken kidneys where a biopsy would be uninformative

4 Hypertension or renovascular disease

5 Pyelonephritis and reflux nephropathy

Front 54

CKD sx

Back 54

- Uraemic symptoms such as anorexia, vomiting, restless legs, fatigue, weakness, pruritus, bone pain. In women ask about amenorrhoea, in menimpotence.

- Oliguria,dyspnoea, ankle swelling.

Front 55

RCC definition, epi, s/s

Back 55

- Arises proximal renal tubular epithelium

- 90% of renal cancers, mean onset 55yr, M:F 2:1

- 50% incidental find

s/s: haematuria, loin pain, abdo mass, cancer signs, fever unknown orig, rarely compress L.renal vein=>L varicoele

- 25% have mets at presentation

- Inc BP from inc renin

Front 56

Lactotrophic pit adenomas s/s epi

Back 56

- 30% of secretory pituitary adenomas

- Produces prolactin (physiological hyperprolactinaemia occurs in preg)

- High levels of prolactin suppress GnRH=>dec FSH and LH which explain many of the sympts Symptoms:

- Men → gynecomastia, decreased libido, infertility, erectile dysfunction, soft testes

- Women → galactorrhea, anovulation (infertility), osteoporosis, oligomenorrhoea

- Both → CNS compression causing headaches, nausea, → Muscle weakness (decreased muscle mass) Loss of body hair

*7% mixedlacto and somatotroph (mammosomatotroph)

Front 57

Somatotroph pit adenomas

Back 57

- Growth hormone producing

- Pre epiphyseal closure → gigantism: proliferation of chondrocytes

- Post epiphyseal closure → acromegaly: proliferation of soft tissues

* Hands and feet

* Bones in face → jaw and prominent brow *Heart

* Carpal tunnel

* Diabetes → HTN

* Colorectal cancer

* Renal failure

* Oily skin and sweating

* inc Skin tags

* Arthritis

* Headache

* Deepening male voice

Front 58

Thyrotrophic adenomas

Back 58

1% of hyperthyroidism, very rare Produces TSH → central hyperthyroidism Usually present as macroadenomas

Front 59

Gonadotrophic adenomas

Back 59

- Usually don’t present with gonadotrophic symptoms but instead mass effects (macroadenoma)

- Rarely presents with menstrual disturbances - Rare

- Elevated gonadotropin levels despite normal or elevated oestrogen levels (which would normal cause negative feedback and suppression)

- Gonadotropinomas most often are asymptomatic because they secrete inactive follicle-stimulating hormone (FSH) and luteinizing hormone (LH)-like glycoproteins and/or alpha subunit.

Front 60

Non functioning pituitary adenoma

Back 60

- Most common pituitary adenoma (25-30%)

- Presents with mass effects (headaches, nausea, bitemporal hemianopia, radiographic abnormalities of the sella turcica, including sellar expansion, bony erosion, and disruption of the diaphragma sella)

Front 61

Hypopituitary sx of non-functioning macroadenoma

Back 61

· ACTH deficiency: Symptoms include fatigue, low blood pressure, weight loss, weakness, depression, nausea, or vomiting

· TSH deficiency: Symptoms include constipation, weight gain, sensitivity to cold, decreased energy, and muscle weakness or aching

· FSH and LH deficiency: In women, symptoms include irregular or stopped menstrual periods and infertility. In men, symptoms include loss of body and facial hair, weakness, lack of interest in sexual activity, erectile dysfunction, and infertility

· GH deficiency: In children, symptoms include short height, fat around the waist and in the face, and poor overall growth. In adults, symptoms include low energy, decreased strength and exercise tolerance, weight gain, decreased muscle mass, and feelings of anxiety or depression

· Prolactin deficiency: In women, symptoms include lack of milk production, fatigue, and loss of underarm and pubic hair. No symptoms are seen in men

· ADH deficiency: Symptoms include increased thirst and urination

Front 62

2o adrenal insuff

Back 62

- Abrupt withdrawal fromchronic steroid use.

- Exogenous administration of steroids =>suppression HPA axis, there is a reduction in cortisol + androgen + ACTH levels

- Aldosterone levels typicallyremain normal because of stimulation from the RAAS.

- To avoid, taper steroids

Front 63

Causes of hyperparthyroid

Back 63

~80% solitary adenoma

~20% hyperplasiaof all glands

<0.5% parathyroid cancer.

Front 64

Hyperparathyroid presentation

Back 64

- Often asymptomatic with inc. blood calc

- Signs relate to inc. ca2+: weak, tired,depressed, thirsty, dehydrated-but-polyuric (osmotic diuresis); renal stones, abdominal pain, constipation (absobtion of more fluid from poo b/c polyuria, also dec. motility b/c of calc) pancreatitis (auto activation of enzymes) + ulcers (inc acid secretion) (duodenal:gastric≈7:1).

- Inc. BP

- Bone resorption effects of PTH=> pain, fractures, osteopenia/osteoporosis

Front 65

Hypoparathyroid 1o definition, s/s, aetiology

Back 65

- PTH secretion is dec. d/t gland failure.

Signs: Those of hypocalcaemia (cramps, confusion, depression) ± autoimmune comorbidities

Causes: Autoimmune; congenital (Di George synd., OHCS

Front 66

2o hypopara aetiology

Back 66

- Radiation, surgery (thyroidectomy, parathyroid-ectomy), hypomagnesaemia (magnesium is required for PTH secretion).

Front 67

Pseudohypoparathyroid def, s/s

Back 67

- Failure of target cell response to PTH

- Signs: Shortmetacarpals (esp. 4th and 5th, fig 2), round face, short stature, calcified basal ganglia, dec IQ

Front 68

Pseudopseudohypoparathyroidism definition

Back 68

The morphological features of pseudohypo-parathyroidism, but with normal biochemistry. The cause for both is genetic.

Front 69

Osteoporosis epi, RFs

Back 69

In those >50yrs: 6%M, 18%F

RFs: parental hx, >4 alcohol units daily, RA, BMI <22, prolonged immobility, untreated menopause

Front 70

Renal osteodystrophy/uraemic osteopathy

Back 70

- Chronic renal failure +

*osteomalacia/ricketts

*2o hyperpara=>bone resorption, osteosclerosis, soft tissue + vascular calc (d/t high phosphate precipitating w calcium), brown tumours

Front 71

Osteititis fibrosa cystica

Back 71

Hyperpara=>chronic inc PTH=>+renal failure, uncontrolled/loss of negative feedback=>inc. action of osteoclasts and resorption of bone=>bone replaced by fibrous tissue (peritrabecular fibrosis)=>brown tumours

- Inc Ca2+, inc PTH

- Fractures, kidney stones, nausea, moth eaten bone

- Appetite/weight loss

Front 72

Adynamic bone disease

Back 72

- Low bone turnover w/o osteoid accumulation

- Decreased no of osteoblasts, no peritrabecular or marrow fibrosis (in contrast to osteitis fibrosa)

- rate of collagen synth by osteoblast and mineralisation collagen both subnormal

- That distinguishes it from osteomalacia when mineralisation defect>defect in bone formation=>relative collagen excess

Front 73

Cerebral/renal salt wasting syndrome

Back 73

- Exact aetiology not know

- Intracranial injury: SAH, TBI, tumour

- XS urine output with high Na+/Cl-

- Needs evidence of hypovolaemia, +/- hyponatraemia

Front 74

Cerebral/renal salt wasting syndrome mgmt

Back 74

- Exclude other causes

- Replace Na+

- Replace fluid losses

+/- fludricortisone