Endocrinology Flashcards
1
Q
Causes of hyperthyroidism
A
Graves disease
Thyroid adenomas (solitary or multinodular)
Postpartum thyroiditis
Aminodarone induced hyperthyroidism
Ectopic thyroid tissue
Exogenous (levothyroxine, excessive iodine, contrast)
De Quervain’s thyroiditis
2
Q
What is De Quervain’s thyroiditis? What are specific/prominent signs and symptoms? How is it treated differently? What should be watched for?
A
Transient hyperthyroidism post viral infection
Neck pain and fever at onset. Thyroid tenderness. Raised esr
Treat with aspirin and steroids.
Watch for following hypothyroidism
3
Q
Generic symptoms of hyperthyroidism
A
Weight loss Increased appetite Palpitations Heat intolerance Irritability Anxiety Tremor Diarrheoa Goitre Oligomenorrhoea
4
Q
Generic signs of hyperthyroidism
A
Tachycarida / AF Full pulse Warm Hyperkinesis Lid-lag (upper eyelid not following down as eye looks down revealing sclera above iris)
5
Q
What is graves disease?
A
Autoimmune condition where antibodies stimulate tsh receptors
6
Q
What signs differentiate graves disease from other forms of hyperthyroidism?
A
Eye signs - proptosis/exopthalmos, lid retraction, optic nerve atrophy, pain, grittiness, conjunctival swelling
Pre-tibial myxoedema
7
Q
What is a bad prognostic indicator for eye signs in graves disease?
A
No protrusion - higher pressure!
8
Q
What blood abnormalities are seen in graves disease other than the normal TFTs?
A
Raised tsh receptor antibodies
Raised antithyroid peroxidase (tpo)
9
Q
What is the clinical course of graves disease?
A
Fluctuating
10
Q
What examination findings and tests would suggests a nodule (single or multiple) is responsible for hyperthyroidism?
A
Can feel nodules!
Radioactive iodine shows hot nodules
Poor response to carbimazole and constant symptoms
11
Q
General treatments for hyperthyroidism
A
Carbimazole Propulthiouracil (ptu) Beta blockers Radioactive iodine Thyroidectomy
12
Q
How does carbimazole work?
What is its t1/2? What consequence is this? Serious adr?
A
Inhibits t3/t4 formation
Weeks - takes a while to work
Agranulocytosis
13
Q
What should patients on carbimazole immediately report to a dr?
A
Mouth ulcers
Sore throats
14
Q
What should be done prior to radioactive iodine therapy or thyroidectomy?
A
Render the patient euthyroid first
15
Q
Compliactions of thyroidectomy
A
Laryngeal nerve palsy
Hypoparathyroidism
Transient hypocalcaemia
Hypothyroidism
16
Q
Signs and symptoms of thyroid storm
A
Pyrexia Tachycardia Restlessness Hypertension Cardiac failure Liver dysfunction
17
Q
What can trigger a thyroid storm?
A
Stress
Infection
Surgery
Radioactive iodine therapy
18
Q
Treatment of thyroid storm
A
Propanolol
Potassium iodide
Carbimazole
Corticosteroids
19
Q
Risks of hyperthyroidism during pregnancy?
A
Graves - mothers antibodies effect fetus - manage by treating mother
Use ptu in first trimester as carbimazole has rarely been teratogenic
20
Q
Side effect of ptu?
A
Hepatotoxicity.
21
Q
What regimes of antithyroid drugs can be used to treat hyperthyroidism?
A
Use carbimazole or ptu to lower thyroid hormones to normal levels
Block thyroid hormones completely and replace with thyroxine
22
Q
Causes of hypothyroidism?
A
Hashimotos thyroditis Postpartum thyroiditis Primary atrophic hypothyroidism Iodine deficiency Drugs - carbimazole, ptu, amiodarone, lithium Hypopituitism
23
Q
Presentation of hypothyroidism?
A
Dry hair Weight gain Cold intolerance Bradycardia Depression Goitre Constipation Myxoedema Tiredness Anaemia Amenorrhoea
24
Q
What would hashimoto’s thyroiditis present with on bloods?
A
Raised tsh
Normal or decreased t3/4
TPO antibodies
Anaemia (of chronic disease)
25
What is a myxedema coma? How does it present?
Decompensated hypothyroidism often following acute insult (infection, stroke)
Confusion to coma
Hypothermia
Cardiac failure (bradycardia and low stroke volume)
Hypoglycaemia
Hyponatremia (decreased Na/katpase in kidneys)
Hypoventilation with T2 respiratory failure
26
Treatment for myxedema coma
```
ABCDEs inc ventilation
IV T3
Steroids
Glucose and sodium as required
Passive rewarming
```
27
Why are steroids used in the treatment of myxoedema coma? What raises suspicion of need?
Incase it is secondary to hypopituitarism with associated adrenal insufficiency
No previous thyroid surgery, no previous goiter
28
Why is t3 used in myxoedema coma not t4. Risks?
T3 is active thus much faster action.
| Higher risk of hyperthyroid issues like arrhythmia
29
General treatment for hypothyroidism
Thyroxine
30
What patients should get a lower starting dose of thyroxine?
Elderly
Long standing disease
IHD patients
31
How long after starting thyroxine would you expect symptom resolution?
6 months
32
What are four main diabetic eye changes?
Blurring due to high sugar
Cateracts
Diabetic retinopathy
Maculopathy
33
What are the subdivisions and features of diabetic retinopathy
Background - microaneurysms (small red dots), superficial haemorrhage (blots), hard exudates (small yellow/white blobs), cotton wool spots (oedema from infarcts)
Proliferative - blood vessels on retina surface, retinal fibrosis and detachment, surface haemorrhages, blood in vitreous humour
34
What is diabetic maculopathy?
Anurysms form and lead causing fluid, fat and protein deposition (oedema and exudate) with central loss of vision
35
Treatment option for diabetic retinopathy and maculopathy? Outcome?
Aggressive sugar control
| Laser treatment - stops progression but doesn't reverse
36
What is the mechanism behind diabetic kidney disease?
Glomerular damage with
- thickened basement membrane
- detached podocytes
- scarring
37
What is the physiological consequence of diabetic kidney disease?
Diabetic nephropathy
| - proteinurea, hypoalbuminia, oedema
38
Is eGFR typically effected in early diabetic kidney disease?
No
39
What is an early sign of diabetic kidney disease? What treatments are important?
Microalbuminuria
Aggressive diabetes control
Ace inhibitors even in presence of normal BP
40
Mechanisms behind diabetic neuropathy?
1 - Uptake of glucose independent of insulin into neurones and schwann cells through glut3. Glucose - sorbitol catalysed by aldose reductase. High sorbitol interferes with neuronal conduction and mylination.
2 - Microvascular damage by non enzymatic glycosylation and vasoconstrictors reduces neuronal perfusion
3 - Oxidative stress from increased ROS production
41
Clinical pictures of diabetic neuropathy?
Symmetrical sensory neuropathy
Painful neuropathy
Mononeuropathy
Autonomic neuropathy
42
How are nerves physically effected in diabetic neuropathy?
demylination then axonal degridation
43
Senses lost in diabetic symmetrical sensory polyneuropathy
Vibration
Pain
Temperature
Proprioception
44
What complications result of a diabetic autonomic neuropathy?
Vagal neuropathy - tachycardia, gastroparesis
Sympathetics to blood vessels - postural hypotension
Nerves to bladder - incomplete emptying, stasis
Nerves to sexual organs - impotance
45
Causes of impotance in diabetes?
```
Neuropathy
Anxiety/depression
Vascular
Medications
Unrelated to diabetes at all!
```
46
Which sign of background diabetic retinopathy suggests proliferative retinopathy is imminent?
Cotton wool spots
47
What comorbidity should be aggressively treated in a patient with diabetic nephropathy
Htn
48
What are major complications of diabetic sensory neuropathy?
Lack of injury sense in foot leading to ulcerations, gangrene and amputation
Charcot arthropathy - microtrauma not detected resulting in chronic fractures and subluxation. Autonomic neuropathy causes hyperaemia and thus increases osteoclast activity causing bone destruction.
49
Differentials for charcots arthropathy?
```
DM
Syphillis
Leprosy
Spinal cord injury
Chronic alcoholism (b12 deficiency)
```
50
Features of charcots arthropathy
```
Deformity
Swelling
Pain
Erythema
Warmth (key! Check temp)
Decreased sensation
```
51
Treatment of charcots arthropathy
Fitted boots
Diabetic control
Surgery to reduce ulceration risk if extremity in bad position
52
What sort of pain do patients with diabetic neuropathy often experience?
Electrical
53
What is the key pathological mechanism for diabetic macrovascular disease?
Injury to arterial wall
Chronic inflammation
Athrosclerosis
54
In addition to athroscleosis what other pathological mechanisms play a role in diabetic macrovascular disease?
Hypercoagubility
Impaired nitric oxide generation
Impaired fibrinolysis
Comorbidites - metabolic syndrome!!
55
Key macrovascular disease in diabetes?
CVD
Stroke
HTN
Gangrene
56
What leaves a diabetic at greater risk of a fatal MI as a direct result of the diabetes?
Athrosclerosis and hypercoagubility
Autonomic neuropathy causing tachycardia
Sensory neuropathy decreasing detection
CKD!
57
Treatment options for diabetic macrovascular prophylaxis?
Blood sugar control
Ace i and other htn control
Lipid control
58
When would you start statins in some one with t2dm? What about t1dm?
T2 - qrisk2 >10
| T1 - over 40, diabetic for > 10 years, nephropathy or other risk factor
59
Causes of diabetes?
```
T1DM
T2DM
Gestational
Metabolic
Drugs
Pancreatic disease
Single gene disorders
```
60
Drugs that can cause diabetes?
Steroids
Antipsychotics
Thiazides
61
Metabolic causes of diabetes?
Acromegally
Cushings
Glucagonoma
62
Single gene disorders associated with diabetes
Prader willi
Maternally inherited diabetes and deafness
Insulin receptor mutations
63
Why are diabetics more at risk of infection?
Impaired chemotaxis and phagocytosis
| Impaired superoxide generation
64
What hand sign may diabetics exhibit? Cause? Implication?
Prayer sign - unable to flatten fingers
Cherioarthropathy - thickened skin and limited joint mobility
Implication for anaesthetics
65
Commonest cause of hypoglycaemia in diabetics?
Treatment related
| Insulin/sulphonylureas
66
What happens to long term diabetics with regards to hypoglycaemia?
Hypoglycaemia unawareness
| Decreased glucagon and adrenaline response so no classic warning symptoms
67
Rarer causes of hypoglycaemia?
```
Insulinoma
Paraneoplastic
Postparandial hypoglycaemia
Hepatic or renal failure reducing respective ability to release glucose
Addisons / ACTH deficiency
Drug induced
Alcohol
```
68
What are the characteristic features of a insulinoma?
Whipples triad
- symptoms on fasting and exercise
- with confirmed hypoglycaemia
- relieved by glucose
69
What are causes of postparandial hypoglycaemia?
Excessive insulin for size of meal
Surgery removes food!
Alcohol with meal exaggerates insulin response
70
How dose alcohol cause hypoglycaemia?
Poor nourishment in alcoholics
| Inhibits gluconeogenesis
71
Causes of type 1 diabetes?
Genetic susceptibility (HLA)
Diet
Hygiene hypothesis
Coxsackie virus
72
Presentation of type 1 diabetes?
```
Young
Acute
Weight loss
Polyuria
Polydipsia
Ketoacidotic
```
73
Precipitants of diabetic ketoacidosis
First presentation
Omitting insulin
Incurrent illness
74
What occurs to potassium in diabetic ketoacidosis?
Potassium deficit due to urinary loss
| Lack of insulin means less potassium shifted into cells so appears normal - high in spite of actual deficit
75
Causes of dehydration in DKA?
Osmotic diuresis
| Vomiting
76
What contributes to potassium leaving cells into the ecf in dka?
Lack of insulin decreases nakatpase reducing potassium uptake
Acidosis increases ecf H so increased potassium release in exchange
Increased ecf tonicity pulls water out of cells increasing icf k concentration resulting in K release.
77
What effect does acidosis have on renal handling of k in dka? In what cells is potassium secreted renally?
Decreases k secretion maintaining k in body
| Principal cells
78
Diagnosis of DKA?
Hyperglycaemia (>11)
Kentonaemia or heavy ketonuria
Acidosis
79
Management of DKA?
Fluids - 1L in 1, 2l in 4, 2 in 8, 2 in 12
Stat SC insulin 10 units
FRIVII (0.1unit/kg/hr)
Add glucose once BM
80
When should the FRIVII be switched off in DKA?
| What should be done?
pH >7.3 OR bicarb >18 OR Ketones
81
Complications of DKA?
Hypovolaemic shock
Acidotic coma
DVT
82
Complications of DKA treatment?
Cerebra or pulmonary oedema
Hypoglycaemia
Hypokalaemia
83
Risk factors for T2DM
```
Genetic
Ethnicity - asian, african
Low birth weight
Age
Obesity
Diet
Sedentary lifestyle
Hypertension
High cholesterol
```
84
Presentation of T2DM
```
Old and fat
Insidious
Polyuria
Polydipsia
Weight loss
Candidia infection
Visual blurring
Low energy
Complications (retinopathy, neuropathy, large vessel disease)
```
85
Skin change associated with T2DM?
| Other conditions seen in?
Acanthosis nigricans
| PCOS, Cushings, acromegally, hypothyroid
86
Diagnostic criteria for DM?
Symptoms and one or asymptomatic and 2 of:
- fasting BM >7
- Glucose tolerance test >11
- HbA1c >6.5%
- Random BM >11
87
How is a Glucose tolerance test performed?
12 hr fast followed by 75g glucose. Measure 2 hours later
88
What is happening if someone is just under on a glucose tolerance test (e.g 9)
Impaired glucose tolerance - on the way to DM. Still at high risk of macrovascualr complications
89
What are the diagnostic values for maternal diabetes?
Fasting BM >5.6
| GTT >7.8
90
Conservative management options for t2dm?
Diet - low sugar, high complex carbs, high fibre, low fat, low alcohol
Exercise - both informal and formal
91
Oral medical management of T2DM
```
Biguanides - metformin
Sulfonylureas - gliclazide
Glitazones - piogliazone
Acarboze inhibitors
Gliptins - saxogliptin
SGLT2 inhibitors - dapagliflozin
```
92
Injectiable management of T2DM
GLP1 agonist - exenatide
| Insulin
93
Non drug management of DM (not conservative)
Gastric banding
94
What is a typical management regime for T2DM with failure of 1st and 2nd line options. What would change 3rd line option?
Lifestyle mods
Metformin
Sulfonylurea - use pioglitazone if hypo risk high eg. Driver.
95
If lifestyle and 2 meds are not controlling t2dm what should be considered?
Triple oral therapy
Add insulin
Novel therapies
96
What is HONK?
Hyperosmolar hyperglycaemic state
| Severe hyperglycaemia without ketosis
97
Presentation of honk?
| Include notable absences
Severe dehydration with hyperosmolality
Hypernatraemia
Coma
No ketones or acidosis
98
Treatment of HONK
Isotonic fluids
| Slowly increasing insulin
99
Predisposing factors for HoNK
Glucose rich food
Steroids
Illness
Thiazides
100
What is the mechanism behind PCOS?
Increased GNrH resulting in high LH and low FSH causing androgen secretion but not conversion into oestrogen.
There is also associated insulin resistance
101
Signs and symptoms of PCOS
```
Hirtuism
Irregular or absent periods
Infertility
Acne
Obesity
Virilisation (baldness, clitoromegally)
```
102
Complication of PCOS?
Metabolic syndrome
103
What investigations should be done in suspected PCOS? What would you expect to see? Pitfalls?
Serum testosterone - high - must check for sex hormone binding globulin
LH - low - depends when taken as pulsetyle
USS - polycystic ovaries
104
Diagnostic criteria for PCOS
2 of
- clinical evidence of hyperandrogenism
- oligo or anovulation
- polycystic ovaries on USS
105
Treatment for PCOS?
Symptomatic - hair removal
Conservative - exercise, diet
Medical - OCP, spironolactone, metformin
106
What OCP to use in PCOS? What is the active ingredient? How does it work?
Dianette - cyproterone acetate
| Progesterone - an antiandrogen
107
Why give PCOS spironolactone?
Antiandrogen properties hence side effect of gynacomastia
108
Why give PCOS metformin?
No only helps with insulin resistance but also with menstrual regularity and infertility
109
Differentials for PCOS for hirsutism?
Idiopathic hirsutism
Congenital adrenal hyperplasia
Cushings
Virilizing tumour of ovary or adrenal
110
What causes congenital adrenal hyperplasia?
Lack of enzyme in steroid metabolism that usually converts progesterone into aldosterone and cortisol. Causes a deficiency in aldosterone and cortisol with an excess in androgens as progesterone is pushed down this pathway.
Lack of cortisol causes high ACTH and thus adrenal hypertrophy
111
How does congenital adrenal hyperplasia present at birth if severe?
```
Ambiguous genitalia in females (cliteral hypertrophy, fused labia)
Adrenal crisis (hypotension, hypoglycaemia)
Mineralcorticoid deficiency (hypotension, hyponatraemia)
```
112
If not too severe, how would congenital adrenal hyperplasia present in adult life?
Precocious puberty
Hirsutism
Primary amenorrhoea
113
How can you test for congenital adrenal hyperplasia?
Administer ACTH and measure response
114
Treatment of congenital adrenal hyperplasia?
Replacement of glucocorticoids and mineralocorticoids
| Genetic councilling
115
In diabetes glucose is found in the urine? Why? How is it normally dealt with by the kidney?
Freely filtered at the glomerulus so [high] in blood means the same in urine exceeding the transport maximum.
Usually glucose is reabsorbed in the PCT fully. On the luminal membrane using a glucose:Na cotransporter (SGLT2) and using Na/K ATPase with GLUT1/2
116
When are serum cortisol levels highest? Lowest? What can change the cycle?
High early morning
Low at midnight
Stress will cause a raise
117
What inhibitory trophic hormones are released by the hypothalamus into the portal circulation? What do they inhibit?
Dopamine - prolactin
| Somatostatin - gh, tsh
118
Local effects of a pituitary tumour?
Compression of optic chiasm - bitemporal hemianopia
Compression of cavernous sinus - CN III, IV and VI dysfunction
Meningeal irritation - headache
Compression of hypothalamus - appetite, sleep, thirst disturbance, DI
Compression of ventricles - hydrocephalus
Sphenoid sinus invasion - csf rhinorrhoea
119
Effects of CN3,4 and 6 dysfunction in cavernous sinus compression?
3 - SR, IR, MR, IO, LPS, sphincter pupillae - ptosis, eye down and out, fixed dilated pupil
4 - SO - diplopia on looking down
6 - LR - cant abduct
All three together causes completely immobile eye
120
Causes of hypopituitarism?
```
Tumour
Sheehans syndrome following post partum haemorrhage
Infections
Trauma
Sarcoidosis
Radiation/chemotherapy
Anorexia nervosa / starvation
```
121
Zones of the adrenals with what they produce?
Zona glomerulosa - mineralocortiocoids
Zona fasicularis - corticosteroids
Zona reticularis - androgens
122
Major effects of glucocorticoids
```
Gluconeogenesis
Protein catabolism
Fat and glycogen deposition
Sodium retention and potassium loss
Immunosuppression
```
123
How does negative feedback work on the hpa axis?
Cortisol inhibits CRH and ACTH formation
124
When should basal cortisol and acth levels be taken? What consideration?
At peak between 0800 and 0900
| Stress should be minimised
125
What main tests are used in patients with high levels of cortisol to determine cause? How do they work?
Dexamethasone suppression tests
Low dose - patients with Cushing's syndrome will not significantly suppress cortisol on administration of dexamethasone
High dose - patients with Cushing's disease will significantly suppress cortisol indicating cause is likely ectopic or adrenal if failed to suppress
126
If cortisol levels are low what main tests can be used to identify the cause? Differentiate them.
Synacthen
Short - if no response to ACTH confirms hypoadrenalism but could be primary, secondary or iatrogenic
Long - if no response suggests primary adrenal failure
127
Why does secondary hypoadrenalism result in a positive short synacthen test? Why does this change with a long one?
Adrenal atrophy
| On a long test the adrenals are kicked into life unless there is a primary pathology
128
What CLINICALLY would differentiate addisons from secondary hypoadrenalism?
Pigmentation from high ACTH
| Low mineralocorticoids producing hypotension and electrolyte imbalance
129
What tests can be used in suspected addisons disease (generally)
```
Random cortisol
Synacthen tests
U+Es
BM
Adrenal antibodies
Abdo xray
Serum aldosterone
```
130
What might be seen in an abdominal xray of an addisons patient?
Calcified adrenals
| Evidence of tb
131
Causes of addisons disease?
```
Autoimmune
TB
Surgical removal
Haemorrhage/infarction
Malignant destruction
```
132
Causes of secondary hypoadrenalism
Exogenous steroids
| Pituitary disease
133
Emergency management of addisons crisis?
NaCl
Hydrocortisone
Glucose
134
Long term treatment of hypoadrenalism?
Gluticorticoids - e.g. Hydrocortisone
| Mineralocorticoids - e.g. Fludrocortisone
135
What is the most common cause of cushings syndrome?
Exogenous steroids
136
What are causes of cushings syndrome?
Iatrogenic
Disease - increased ACTH from pituitary
Atopic ACTH from a tumour
Endogenous cortisol secretion from adrenals
137
A patient with a history of cushing type symptoms has a positive low dose dexamethasone suppression test. What tests will help diagnose the source?
```
Adrenal ct
Pituitary mri
K levels
High dose dexamethasone test
Plasma acth
Cheat xray
```
138
A patient with a history of cushing type symptoms has a positive low dose dexamethasone suppression test. A high dose dexamethasone suppression test is negative, his potassium is normal and there are no signs on the chest xray. A ct of adrenals is negative and there is nothing on a pituitary mri. Where is the likely lesion? Why?
Pituitary. Most acth secreting tumours are too small to see on mri. Normal potassium suggests not ectopic and a response to the high dose tests suggests a pituitary source.
139
What causes death in untreated cushings?
Htn with mi and heart failure
| Infection
140
How is cushings treated?
Ketoconazole to reduce plasma cortisol
Removal of source if possible
If not bilateral adralectomy with replacement
141
What is the risk with bilateral adrenelectomy for cushings?
Nelsons syndrome
| No feedback so massive enlargement of pituitary
142
Hazards to discuss on starting steroids for any condition
```
Infection
Suppress own steroids
Hypertension
Pancreatitis
Weight gain
Diabetes
Depression
Osteoporosis
Thin skin and bruising
Cataracts
```
143
What is diabetes insipidus?
Deficiency ir insensitivity to adh resulting in polyurea, nocturea and compensatory polydipsia
144
What is the biochemical profile of diabetes insipidus?
High plasma osmolality
Low urine osmolality
High plasma sodium
High urine volumes
145
You suspect diabetes insipidus. How do you test for it?
Water deprivation test for up to eight hours
Plasma osmolality should stay the same whilst urine osmolality should increase in a normal person.
If this does not occur sufficiently give synthetic ADH (desmopressing) and monitor change to differentiate cranial from renal.
146
When should a water deprevation test be stopped?
If >3% body weight reduction
147
Causes of cranial diabetes insipidus?
```
Hypothalmic-pituitary surgery
Trauma
Infection
Tumour
Necrosis - sheehans
Famililal
Idiopathic
```
148
Causes of nephrogenic diabetes insipidus
```
Familial
Idiopathic
Renal disease
Lithium
Hypokalaemia
Hypercalcaemia
Sickle cell disease
```
149
Treatment of cranial diabetes insipidus
Desmopressin
150
Treatment of nephrogenic diabetes insipidus
Reverse cause if possible
151
Other causes of polyuria and polydipsia not diabetes insipidus
Diabetes mellitus
Hypokalaemia
Hypercalcaemia
Primary polydipsia - psychiatric, too much water, low plasma osmolarity
152
How does SIADH present?
Dilutional hyponatraemia with low plama osmolality
Euvolemic with no hypotension
Normal potassium
No response to 1-2 L of 0.9% sodium chloride
153
Treatment of SIADH
Fluid restriction
Demeclocycline to inhibit adh
Cautious use of hypertonic saline in severe illness
154
Causes of siadh
```
Tumours
Pneumonia
Head injury
Alcohol withdrawal
Drugs carbamazepine
```
155
Causes of hyponatraemia with hypovolaemia?
Vomiting, diarrheoa, burns, haemorrhage, osmotic diuresis, diuretics, addisons,
156
Causes of hyponatraemia with euvolaemia?
```
SIADH
Overenthusiastic 5% glucose use
Exertion with only water replacement
psychogenic polydipsia
Desmopressin
Addisons
Mannitol
Sickle cell syndrome
```
157
Causes of hyponatraemia with hypervolaemia
Heart failure, liver failure, hypoalbuminaemia
158
What is the mechanism behind hyponatraemia with hypovolaemia with respect to adh.
Loss of salts out of proportion to loss of water causing low osmolarity
Due to volume depletion adh still released to maintain volume lowering osmolarity further still
159
What are signs and symptoms of very low sodium concentrations? What sort of values do they occur at? Why do they occur?
Caused by water moving into neurones - hyponatraemic encephalopathy
160
Who are most at risk of hyponatraemic encephalopathy?
Children,
Premenopausal women
Hypoxaemic patients
161
What should be done in a patient with hyponatraemia with euvolaemia to further diagnose?
Plasma and urine electolytes and osmalarities
| Screen for addisons and siadh
162
Treatment of hyponatraemia with euvolaemia
Fluid restriction
Slow 0.9% nacl
Severe neurological signs - hypertonic saline
163
Causes of hypernatraemia?
```
Water deficite (impaired thirst, unable to drink, diabetes insipitus, osmotic diuresis)
Excessive sodium administration (NaCl overuse, drugs with high na content)
```
164
Symptoms of hypernatraemia?
```
Nausea
Vomiting
Fever
Confusion
Polydipsia
```
165
Investigations of hypernatraemia
Urine and plasma osmolality and sodium
166
Symptoms and signs of acromegally
Bone - pronounced brow, wide nose, large jaw, macroglossia, wide spaced teeth, large hands and feet
Skin - acanthosis nigracans, darker skin, curly hair
Physiological - snoring, OSA, DM, HTN, headaches, decreased libido, carpal tunnel
167
Tests in suspected acromegally
Glucose tolerance test - +ve with failed suppression of growth hormone
MRI pituitary
168
Treatment of acromegaly
Lesion removal
Somatostatin analogues
GH antagonist
169
Causes of hyperprolactinaemia
Pituitary adenoma secreting prolactin
Compression of pituitary stalk
Medications - antipsycotics, metaclopramide, ecstacy
Physiological - pregnancy, breastfeeding
170
Presentation of hyperprolactinaemia
Female - amenorrhoea, oligomenorrhoes infertility, galactorrhoea
Male - galactorrhoea, impotence, hypogonadism,
Both - osteoporosis,
171
Test in suspected hyperprolactinaemia
Prolactin levels between 8 and 160
| Pregnancy test
172
Differentiate cause of hyperprolactinaemia from prolactin levels
>5000 from prolactinoma
| >10000 from macroprolactinoma
173
Treatment of microprolactinoma
Dopamine agonist eg bromocryptine
174
Treatment of macroprolactinoma
Bromocriptine
| If no response and visual symptoms etc then surgery
175
Causes of diabetes insipidus
Cranial - idiopathic, trauma, congenital, tumour, haemorrhage
Renal - inherited, lithium, ckd, hypokalaemia
176
Tests to run in suspected diabetes insipidus?
DM screen
U+E
Serum and urine osmolarities
177
What changes in osmolarity would you see in urine and plasma (and ratio!) in diabetes insipidus?
Raised plasma
Lowered urine
U:P ratio
178
Diagnostic test for diabetes insipidus
Water deprivation test - urine should normally concentrate
| If it fails to give desmopressin and urine should then concentrate if cranial and not if nephrogenic
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Differentials of diabetes insipidus
DM
Lithium
Diuretic use
Primary polydipsia
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Treatment of diabetes insipidus
Cranial - desmopressin, treat cause
| Renal - treat cause, nsaids, bendroflumethiazide
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Commonest hormones secreted by pituitary tumours
Prolactin
ACTH
GH
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A patient with a know pituitary tumour presents with sudden headache, meningism and visual field defect. What should be considered?
Pituitary apoplexy - bleed into tumour
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Features of growth hormone deficiency
Loss of muscle, difficulty exercising, decreased cardiac output, low glucose, osteoporosis
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Treatment of gh deficiency
Somatotrophin
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Causes of primary hyperaldosteronism
Adenoma - conns
| Bilateral adrenocortical hyperplasia
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If someone has hyperaldosteronism but their k is nor,al what other blood test will be deranged?
Alkalosis
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What should be tested in suspected hyperaldosteronism
U+e
| Renin and aldosterone levels
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What tests to run on a patient with proven primary hyperaldosteronism?
Mri
| If adrenal mass seen take adrenal vein sampling bilat to see if it the source
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Treatment of primary hyperaldosteronism?
Conns - remove adenoma
| Spironolactone
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Causes of secondary hyperaldosteroneism
High renin due to low renal perfusion
Renal artery stenosis
Diuretics
Ccf
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What is the 10% rule in phaeochromocytomas
10% malignant, extra adrenal, bilateral, familial
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Where are most extraadrenal phaeochromocytomas
Aortic bifurcation
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Who should be screened for thyroid problems?
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AF
Hyperlipidaemia
Lithium
DM
Amiodarone
Downs
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What independantly influences prognosis and risk of thyroid eye disease
Smoking
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What causes a goitre in hashimotos?
Wbc infiltration
