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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

define endocrine and exocrine

A

endocrine put inngs into teh blood
exocine purs yjomgs inot the sight o action - for example into the stomach

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2
Q

what are teh differences between water and fat soluble hormones

A

water:

half life - short
clerance - fast

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3
Q

what are peptide hormones

A

tey vary in amino acid lengths
they may bind t a carbohydrate
released in pulses or bursts
stored in secretory granules
cleared by tissues and circulating enzymes

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4
Q

how are peptide hormones stored

A

preprohorme
prehormone
stored as a horone
secreted as a hormone

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5
Q

what are the 4 catogries of hormones

A

peptides
Amines
iodothyronines - not water soluble
sterioid - not water soluble

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6
Q

how are iodothyronins made

A

Secretory cells release thyroglobulin into colloid – acts as base for thyroid hormone synthesis

Incorporation of iodine on tyrosine molecules to form iodothyrosines

Conjugation of iodothyrosines gives rise to T3 and T4 and stored in colloid bound to thyroglobulin

TSH stimulates the movement of colloid into secretory cell, T4 and T3 cleaved from thyroglobulin

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7
Q

which hormoes are in teh nucluer receptro family

A

oestrogen, thyroid hormone, vit D

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8
Q

how does vitamin D work inside the cell when it gets t teh recepotr

A

Fat soluble
Enters cells directly to nucleus to stimulate mRNA production
Transported by Vitamin D binding protein

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9
Q

what is the rhythem of cortisol called

A

diruinal rhythems

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10
Q

what are the functions of thyrid hormones

A

Accelerates food metabolism
Increases protein synthesis
Stimulation of carbohydrate metabolism
Enhances fat metabolism
Increase in ventilation rate
Increase in cardiac output and heart rate
Brain development during foetal life and postnatal development
Growth rate accelerated

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11
Q

what are teh three layers of teh adrenals and what do they produce

A

Zona glomerulosa - mineralcorticoids (Aldosterone)
Zona fasicilata - glucocorticoids (cortisol)
Zona reticularis - androgens (sex hormones - dihydroepiandrosterone)

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12
Q

what are the BMI weight catogries

A

<18.5 underweight
18.5 - 24.9 normal
25.0 - 29.9 overweight
30.0 - 39.9 obese
>40 morbidly obese

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13
Q

what are teh risks caused by obesity

A

Type II diabetes
Hypertension
Coronary artery disease
Stroke
Osteoarthritis
Obstructive sleep apnoea
Carcinoma:
Breast
Endometrium
Prostate
Colon

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14
Q

what hormone inhibits hunger and another ne

A

leptin - it is expressed in white fat
it is immunostimulatory

Insulin as well

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15
Q

what is an additional hormone that inhibits appetite

A

cholecystokinin - CCK

receptors in teh pyloric sphincyer and delayes gastjc empyting

it is an enterogastrone

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16
Q

what is teh main appitite stimulator and another one

A

ghrelin

agouti releated peptide

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17
Q

what is PYY

A

binds to NPY receptrs, and is secred by ilium, pancrse and colon

it inhibits gastic motility and reduced appetite

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18
Q

what is release when teh stomach is full stimulate satiety

A

CCK
GLP1 (glucagon like peptide)
Insulin
PYY (peptide YY)

Leptin is tehn produced longer term

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19
Q

what are teh hormones produced by teh anteriro pituitry

A

FLAT PIG

1.Follicle-stimulating hormone (FSH):
- Produced in gonadotrophs
2. Lutenizing hormone (LH):
- Prodcued in gonadotrophs
3. Adrenocorticotropic hormone (ACTH - also known as corticotropin):
- Produced in corticotrophs
4. Thyroid-stimulating hormone (TSH - also known as thyrotropin):
- Produced in thyrotrophs
5. Prolactin:
- Produced in lactotrophs
6. IGNORE
7. Growth hormone (GH - also known as somatotropin):
- Produced in somatotrophs

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20
Q

What are the three things ot think about when it comes to pituitry tumours

A

-pressure on local structure for example the optci nerve or 4th ventricle
-pressure on the normal pituitry
-functioninf tumour - it releases hormones
-

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21
Q
  • How to differentiate between CSF and snot
A

CSF has glucose in it

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22
Q

what are the three types of functioning pituitry tumour

A

prolatinoma
acromegally and giganism
cushings diseas

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23
Q

why does acromegally cuase suhc large growth when just givign growth homone doesnt have such an effect

A

gigantism growth hormone also surpresses the rest of the pituitry gland beause there is a tumour, so the children dont go through puberty and the long bones arent inhibited from growing

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24
Q

what is the test to do if someone if infertile and how can it be treated

A

you can do a prolacin test bevause prolacin surpresses other things and make you more infertile

Give a dopamine agonist! this will also cause teh tumour to shrink

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25
Q

what are the signs of cushings in children

A

fat and short

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26
Q

what does thelarche mean

A

breast development

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27
Q

what does thelarche mean

A

breast development

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28
Q

what starts thelarchy

A

induced by estrogne and it happens over three years

Ductal proliferation
Site specific adipose deposition`
Enlargement of the areola & nipple

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29
Q

what is teh shap diffence in a prepubertal and post pubertal uterus

A

pre is tube shap, post is pear shap

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30
Q

diabeteis type 1 defornition

A

Metabolic Disorder characterised by hyperglycaemia due to absolute immunodeficiency. Develops due to destruction og pancreatic beta cells, immune mediated.

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31
Q

diabeties type 1: Epidemiology

Aetiology

Risk Factors

A

5-10% of all diabetes, normally diagnosed between 5-15 years

Autoimmune condition causing destruction of the pancreas, HLA-DR and HLA-DQ provide protection from or increase suspetability to the disease. Enviromental facots trigger destrction of beta cels such as viruses.

Genetic predisposition, geographical region (european), nfection agents, diatry factors

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32
Q

diabeties type 1 pathophysioology

A

Destruction of the pancreas by antibodies, when 80-90% of beta cells have been destroyed, hyperglycemia develops,

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33
Q

Diabeties 1, key signs, signs and symptoms

A

Polyuria, polydipsia, fatuigue

Young age, weight loss, low BMI, Automimmine disease, ketoacidosis

Thirst, dry mouth, blurred vision, hunger, weightloss

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34
Q

diabeties 1 tests

A

Random glucose tolerance test >11.1

Fasting plasma glucose

Glycerated heamogobin A1C test (this measure the glucose attatched t the Hb
>6.5% is diabetes

Low CC peptide (releaed from insulin)

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35
Q

diabeties 1 treatment and monitering

A

Basal blous insulin there is short and long acting which are used

Check BP and treat with a goal of <140/90
When not on statins, check the lipis profile at the initial check and then every 5 years

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36
Q

what are teh macrovascular complication of diabeties 1

A

Macrovascular - CAD (coronary artery dsease), cerebrovascular disease, PAD

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37
Q

what are teh microvascualer complications of diabeties

A

Microvascular - retinopathy, neurophathy, nephropathy, diabetic foot

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38
Q

diabeies 2 defornition, epidemiology, aetiology, risk factors

A

Progressive disorder defined by deficits in insulin secretion and increased insulin resistance that leads to abnormal glucose metabolism

Older age adults

Genetic susceptibility

Diet, obesity, older age, gestational diabetes

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39
Q

whate are the tests for type 2 diabeties

A

Random glucose test in urine

HBA1C test - prediabetes is 42-47, diabetes is 48mmol/l

Oral glucose tolerance test - performed in the morning before any food, there is a fasting plasma glucose taken, then 75g drink, then measuring of glucose 2 hours later . Diabeties is a fastig glucose of >7, prediabeties is a fasting glucose of >6.1-6.9

Random glucose test - if higher than 11mmol/l its diabetes

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40
Q

differential diagosis for type 2 diabeties

A

Type 1, pre diabetes hyperglycaemia, latent autoimmune disease, Cushing’s disease

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41
Q

what is teh treatment and manegment for tpe 2 diabeties

A

Diet and exercise changes

Metformin and gliclazide (this is a sulfonylurea and works by increased the amount of insulin released form the pancreas)

Insulin

Regular HBA1C tests

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42
Q

what are complication of type 2 diabeties

A

Hyperosmolar hyperglyceamic state, diabetic nephropathy, diabetic neuropathy (-> lack of sensation in feet -> occult foot ulcers), diabetic retinopathy, Hyperosmolar hyperglycaemic nonketotic coma (mostly in type 2s)

Increased risk of cardiovascular disease

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43
Q

define ketoacidosis

A

An acute metabolic complication, where the production of ketones causes an acidic pH which can be fatal. Ketones are produced when the body breaks down excessive amounts of fat.

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44
Q

ketoacidosis epidemiology and risk factors

A

Diabeties 1 (nearly always), low carbohydrate diet

inadequate or inappropriate insulin therapy
infection
myocardial infarction
Pancreatitis

having an infection, such as flu or a urinary tract infection (UTI)
not following your treatment plan, such as missing doses of insulin
an injury or surgery
taking certain medicines, such as steroids
binge drinking
using illegal drugs
pregnancy
having your period

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45
Q

ketoacidosis key presintation, signs and symptoms

A

Diabetes, N+V, abdominal pain. Dehydration

Acetone smell on breath

needing to pee more than usual
feeling very thirsty
being sick
tummy pain
breath that smells fruity (like pear drop sweets, or nail varnish)
deep or fast breathing
feeling very tired or sleepy
confusion
passing out

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46
Q

ketoacidosis

A
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47
Q

ketoacidosis tests

A

venous blood gas
blood ketones - lower than 0.6mmol is normal 3 mol is critical
blood glucose
urea and electrolytes

Blood ketone test

urinalysis
ECG
pregnancy test
amylase and lipase

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48
Q

ketoacidosis treatment

A

insulin, usually given into a vein (intravenously)
fluids given into a vein to rehydrate your body
nutrients given into a vein to replace any you’ve lost

Moniter blood glcose and ketones carefully

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49
Q

Hyperosmolar hyperglycaemic state defortion

A

profound hyperglycaemia (glucose ≥30 mmol/L [≥540 mg/dL]), hyperosmolality (effective serum osmolality usually ≥320 mOsm/kg [≥320 mmol/kg]), and volume depletion in the absence of significant ketoacidosis (pH ≥7.3 and bicarbonate ≥15 mmol/L [≥15 mEq/L]), and is a serious complication of diabetes

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50
Q

Hyperosmolar hyperglycaemic state epidemiology and risk factors

A

Type 2 diabetes

infection
inadequate insulin or oral antidiabetic therapy
acute illness in a known patient with diabetes
nursing home residents

It can be the first time someone presents with diabetes and is a form of diabetic crisis, can go alongside diabetic ketoacidosis

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51
Q

Hyperosmolar hyperglycaemic state signs and symptoms

A

acute cognitive impairment
presence of risk factors

polyuria
polydipsia
weight loss
nausea and vomiting

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52
Q

Hyperosmolar hyperglycaemic state tests

A
  • blood glucose (high)
  • blood ketones (low)
  • venous blood gas
  • serum osmolality (high)
  • urinalysis
  • cardiac enzymes
  • chest x-ray
  • liver function tests
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53
Q

Hyperosmolar hyperglycaemic state differential diagnosis

A

Conditions which causes impaired mental state - CNS infection, hypernatremia

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54
Q

Hyperosmolar hyperglycaemic state manegment and moitering

A

intravenous fluids and potassium replacement
PLUS – supportive care and referral to critical care
PLUS – insulin
PLUS – identify and treat any precipitating acute illness

Assess for cerebral oedema and if GCS is low order a head CT scan
Keep under close obstervation

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55
Q

Hypoglycaemia defornition

A

Hypoglycaemia is a clinical syndrome present when the blood glucose concentration falls below the normal fasting glucose range, generally <3.3 mmol/L (<60 mg/dL)

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56
Q

Hypoglycaemia risk factors

A

middle age
female sex
ethanol consumption
bariatric surgery - not absorbing enough?
diabeties

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57
Q

Hypoglycaemia causes

A

It can be diagnosed by wipples trangle which is: symptoms of hypoglycaemia, low blood plasma glucose concentration, and relief of symptoms when plasma glucose concentration is increased

It can also be caused by an insulinoma, which is a insulin secreting tumour.

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58
Q

Hypoglycaemia key, signs, symptoms

A

Diaphoresis (excessive sweating)
anxiety
tremor
hunger

Hypotension, hyperpigmentation, weightloss or gain

Nausea, confusion, tremor, sweating, palpitations, or hunger.

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59
Q

Hypoglycaemia tests

A

serum glucose
liver function testing
renal function testing
serum insulin

48- to 72-hour fast under observation
oral glucose tolerance test
serum insulin-like growth factor (IGF)-II
serum adrenocorticotropic hormone

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60
Q

Hypoglycaemia differential diagnosis

A

Cardiac dysrhythmia. Endocrine disorders (eg, pheochromocytoma, Addison disease, glucagon deficiency, carcinomas, extrahepatic tumors) Substance abuse (eg, cocaine, ethanol, salicylates, beta-blockers, pentamidine) Hypoglycaemic agents (eg, insulin, oral hypoglycemic agents

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61
Q

hypogluceamia manegment and monitering

A

In emergancy, intramuscular glucagon administered to raise BG
Quick acting carhohydrate

Long term:
Dietary changes such as more protien
Psychaitric assessment if due to overdose/toxin/ethanol

Nutrition councelling
Medication chnages that moght be causing it
Tumour removal

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62
Q

hyperthyroid epidemiology and risk factors

A

Affects more females than males, mainly between 20-40 years

Female, family history, stress, smoking, amiodarone

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63
Q

hyperthyroid aitiology

A
  • Graves’ disease - autoimmune disease attacking the thyroid gland causing an excess production
  • Associated with other autoimmune disease - T1DM toxic multilocularities - older women,
  • Toxic multinodular goitre - an engorged thyroid, causing too much hormone to be produced (antithyroid medication radioactive iodine, surgery)
  • Toxic thyroid adenoma
  • Pituitary adenoma
  • De Quervains thyroiditis - swelling of the thyroid gland due to viral infection such as mumps or flu
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64
Q

pathophysiology of graves disease

A
  • Graves’ Disease
    ○ Serum IgG antibodies called TSH receptor stimulating antibodies (TRAb) bind to TSH receptors on the thyroid and stimulate T3/4 production
    This results in excess secretion, hyperplasia of the thyroid follicular cells, hyperthyroidism and goitre
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65
Q

hyperthyroid key, signs and symptoms

A

Heat intolerance, irritability and weight loss

  • Tachycardia/AF
  • Goitre
  • Tremor
  • Hyperkinesia – increase in muscle activity
  • Lid lag
  • Lid retraction
  • Thin hair and hair loss
  • Onycholysis – painless separation of the nail from the nail bed
  • Exophthalmos – bulging of the eye out of the orbit

Insomnia, sialorrhea, Palpitations, fatigue, tremor, anxiety, weight loss, menstrual disturbances

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66
Q

hyperthyroid tests

A

Thyroid function test, (if it is primary disease, it will be low TSH and high T3/T4) if secondary high TSH and high T3/T4

Thyroid ultrasound, radioactive iodine isotope uptake scan

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67
Q

hyperthyroid manegemtn and monitering

A

Beta blockers for heart rate control

Carbimazole - antithyroid drug, which also has immunosuppressive effects, this has two mechanisms, block and replace with thyroxine to get it more tightly controlled, or a strong doe at first which is then reduced in accordance to the tests

Radioiodine therapy (not in pregnancy and breast feeding)

Thyroidectomy - removal of part of the gland

Dose of carbimizol is adjusted in accordance to thyroid tests

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68
Q

hyperthyroid complications

A

Congestive heart failure, atrial fibrillation, osteoporosis, graves dermopathy (elephantiasis) and graves ophthalmopathy complications

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69
Q

what is a thyroid crisis (hyper) and how is it treated

A

There is a rapid deteriorsion of thyrotoxicosis which hyperpyrexia (increased body temp), tachycardia, restlessness, coma and death
Its normally caused by surgery, stress or infection
It can be treated by a large dose of carbimizole, propranolol and hydrocortisone to prevent the conversion of T4-T3
Also potassium iodide to block the release of thyroid hormone form the gland

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70
Q

hypothyroidism defornition

A

Underactivity of the thyroid gland. May be primary (from disease of the thyroid gland) or secondary (pituitary/hypothalamic disease)

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71
Q

hypothyroidism epidemiology

A

Females more than males
Only 0.1-2% of the population
Family history of autoimmune disease

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72
Q

hypothyroidism causes

A
  • Autoimmune thyroiditis - anti thyroid hormones are made and so there is lymphatic infiltration of the gland and eventual atrophy (so no goitre)
    Almost all patients have serum antibodies to thyroglobulin and thyroid peroxidase (TPO)
    Associated with other autoimmune conditions e.g. pernicious anaemia and Addison’s disease
    CD8 mediated
  • Hashimoto thyroiditis - caused by autoimmune, associated with goitre
  • Amiodarone - contains hight levels of iodine and can cause hyperactive thyroid. It is a drug taken for irregular heartbeats and slows the nerve impulses in the heart
  • lithium toxicity - it collects in the thyroid and prevents it from being able to uptake more iodine
  • post-partum thyroiditis
  • Iodine deficiency - common in mountainous areas

Congenital hypothyroidism

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73
Q

hypothyroidism signs (mneumonic)

A

BRADYCARDIC
* Bradycardia
* Reflexes relax slowly
* Ataxia
* Dry thin hair/skin
* Yawning
* Cold hands
* Ascites
* Round puffy face
* Defeated demeanour
* Immobile – ileus (temporary arrest of intestinal peristalsis)
* Congestive HF

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74
Q

hypothyroidism symptoms

A
  • Hoarse voice
  • Goitre
  • Weight gain
  • Constipation
  • Cold intolerance
  • Menorrhagia – heavy periods
  • Tiredness
  • Lethargy
  • Poor memory
  • Puffy eyes
    Arthralgia/myalgia
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75
Q

hypothyroidism tests

A

Thyroid function test

Thyroid antibodies in Hashimoto’s

FBC - anaemia

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76
Q

hypothyroidism differential diagnosis

A

Primary adrenal insufficiency, anaemia,
§ Hyperlipidaemia
§ Hyponatraemia (due to increased ADH and impaired clearance of free water)
Increased serum creatine kinase levels with associated myopath

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77
Q

hypothyroidism treatmetn

A

Levothyroxine T4 started at 25mcg and increased every 4-6 weeks
§ Primary – titrate dose until TSH normalises
§ Secondary – TSH will always be low, T4 monitored

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78
Q

hypothyrpisism complications

A

heart disease, goitre, pregnancy problems and a life-threatening condition called myxoedema coma

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79
Q

thyroid cancer types

A

Papillary - young people
Follicular - middle age
Medullary - familial
Lymphoma - variable
Anaplastic - aggressive

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80
Q

thyroid cancer signs and symptoms

A

Lumps in neck, swollen glands, horarsness, sore throat

Lymph node metastasis, lung or bone metastasis, thyroid nodule which history of growth, hard and irregular nodes, enlarged lymph nodes

Thyroid nodules, dysphagia (difficulty swallowing), hoarse voice

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81
Q

thyroid cancer tests

A
  • Fine needle aspiration cytology biopsy best for distinguishing between benign and malignant thyroid nodules
  • Thyroid ultrasound
  • TFTs – hyper/hypothyroidism needs to be treated before surgery
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82
Q

thyroid cancer treatment for follicular and papillery

A
  • Follicular and papillary cancers
    ○ Total thyroidectomy with neck dissection for local nodal spread
    ○ Ablative radioiodine subsequently given – taken up by remaining thyroid tissue or metastatic lesions
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83
Q

thyroid cancer treatment for anaplastic and lymphoma

A
  • Anaplastic and lymphoma
    ○ External radiotherapy may produce brief respite
    ○ Otherwise treatment is largely palliative
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84
Q

thyroid cancer monitering

A

Long term monitoring o repeat ultrasound examinations, radioactive scanning, measuring thyroglobin level in the blood

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85
Q

cushings syndrome and cushings disease differnces

A

The clinical state of free circulating glucocorticoids

Cushing’s syndrome is the symptoms caused by too much cortisol in the body.
Cushing’s disease is caused specifically by a tumour in the pituitary causing too much ACTH, it is lie the secondary disease version essentially.

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86
Q

cushings syndrome causes

A

Most common cause is oral steroids, increased ACTH, and increased cortisol itself being made randomly by teh adrenals (for example an adenoma)

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87
Q

cushings syndrome signs and symptoms

A

Truncal obesity, moon face, red face, buffalo hump on back, acne, hirsutism (male pattern hair growth in women), this skin and easy bruising, osteoporosis

Cateracts, ulcers, purple striae on skin, hypertention, hyper-glycemua, increased risk of infection, necrosis, glucosuria,

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88
Q

cushings syndrome tests

A

Random cortisol - misleading test though as diurinal rhythem

24 hour urinary free cortisol measurment - not elevated levels make it unlikely to be cushings

overnight dexamethasone test

If plasma ACTH is low, adrenal imading using CT or MRI to detect neoplams
If ACTH is high, if there is suppression by high dose its probably a pituitry adenoma so look for one with an MRI, if there is no surpressio its probl do to ectopic, this involves CT scant of abdo, chest and pelvis, MRI of neck and thorx, chest x ray to look fr lung tumours

Do the corticotrophin releasing hormone test - if cortisol increases it’s a pituitry prblem

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89
Q

cushings syndrome differential diagnosis

A

Diabetes type 2, pseudo Cushing’s - caused by alcohol excess which resloves within 1-3 weeks of abstinence

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90
Q

cushings syndrome treatment and management

A
  • If iantrogenic - stop the steroids
  • If Cushing’s disease - transsphenoidal removal of pituitary
  • Adrenal adenoma - adrenalectomy, radiotherapy
  • Adrenal carcinoma - adrenalectomy and radiotherapy and adrenolytic drugs (mitotane)
  • Ectopic ACTH - surgery to remove tumour if possible

Essentially, remove the tumours and rebalance the hormone levels, its kind of obvious.

If there is an adrenal adenectomy it might causes nelsons disease where the pituitary continues to release ACTH in large amounts which causes bronze pigmentation, visual disturbances, and headaches

Long term steroids if adrenalectomy so measuring the levels of it

91
Q

cushings syndrome how does teh dexamethasone surpression test work

A

Dexamethasone suppression test - there is the low dose and the high dose, the low dose confirms that its Cushing’s and the high dose says if its caused by excess ACTH or excess cortisol from the adrenal

Low dose: you give 1mg of dexamethasone the night before and if it suppresses it when measured on a blood testt at 9am, then its not Cushing’s, as in Cushing’s its used to the levels being so ight all the time that a little more wont make any difference

High dose: 8mg is given - if this is suppressed the Cushing’s is caused by the ACTH from the pituitary, if it is not suppressed and the ACTH is still very high it is caused by an ectopic tumour, and if it’s not suppressed by eth ACTH is low then it is caused by an adenoma.

92
Q

acromegally defornition

A

Acromegaly- excessive production of growth hormones occurring in adults after fusion of the epiphyseal plates

93
Q

gigantism defornition

A

Gigantism - excessive production of growth hormone occurring in children before the fusion for the epiphysis of long bones which causes extra growth

94
Q

aetiology and risk factors for gigantism/acromegally

A

Benign GH producing pituitary adenomas - very slow onsey over many years
Ectopic- GH releasing hormone form a carcinoid tumour

Multiple endocrine neoplasia

95
Q

signs and symptoms of acromegally

A
  • Acral enlargement (growth in the hands, feet, jaw)
  • Big tongue
  • Prominent supraorbital ridg
  • Thick skin
  • Sleep apnoea
  • Hypertension
  • Puffy lips eyelids and skin
  • Headache
  • Bitemporal hemianopia
  • Acro paraesthesia
  • Sweating
  • Arthralgia
  • Decreased libido
  • Amenorrhea
  • Galactorrhoea (random milk production)
96
Q

tests for acromegallly

A

Oral glucose test - a rise in blood glucose should suppress GH levels. If they remain high it is diagnostic for acromegaly

IGF1 level - should be raised in acromegally
MRI - of pituitry fossa
Visual field defects - betemporal hemianopia
Serum prolacteremia - can be raised in the case of an adenoma
ECG and ecocardiogram

97
Q

treatment for acromegally

A

1 - Transsphenoidal pituitry surgery to remove an adeoma, can causes diabetes insipidus, infection, hypopituitrism
2- Somato statin analougen inhibit GH secretion
3- Dopamine agonist inhibit GH secretion
4- GH antagonist
5- External radiotherapy

98
Q

who is prolacteremia most commen in

A

young women

99
Q

what is the aetiology of prolacteremai

A

The most commen cuase is a prolactin secreating pituityr adenoma
Other tuours couls also cuase it by inhibiting dopamine and reducing its inhibitory capabilities
Also primary hyperthyroidism (high TSH stimulates it)
Drugs such as oestrogens and metoclopramide (ant sickness drug)

100
Q

symptoms of prolacteremia

A

Loss of libido
Galactorrhoea
Reduced fertility
Decreased libido
amenhorrhea

101
Q

test and treatment for prolactermia

A
  • Serum prolactin level (at least 3 measurements)
  • Thyroid function tests
  • MRI of the pituitary
  • Dopamine agonist – CABERGOLINE or BROMOCRIPTINE
102
Q

what is a carcinoid tumour

A

Release of serotonin and other vasoactive peptides from a carcinoid tumour
They can be found in the midgut, bronchus and pancreas

They are a subset of neuroendocrine tumour on a whole and usually benign in the digestive tract or lungs

103
Q

risk factors and pathophysiology of carcinoid tu ours

A

Having genetic multiple endocrine neoplasia type 1

Random tumours that secrete hormones such as serotonin

104
Q

signs of carcinoid tumours

A

palpitations
abdominal cramps
Telangiectasia (spider veins)
signs of right heart failure

105
Q

carconoid tumour test

A

serum chromogranin A/B
urinary 5-hydroxyindoleacetic acid
metabolic panel
liver function tests

106
Q

carcinoid tumour treatment

A

Neuroendocrine tumour can be treated with octreotide which is a somatostatin analogue

107
Q

aitiology of hyperaldosternoism - primary and secondary

A

There is two catogries: primary and secondary

hyperaldosteronism causes an increased sodium and decreasde potassium

Primary
* Idiopathic - xona glomerulosa increases number of aldosterone secreting cells
* Conns - tumour in the ZGlom
* Famelial - aldosteone cells start reponsing to adrenocorticotrophic hormone as well as angiotensin 2
Secondary -
* Renin producting tumour
* Heart faliure
Chronic low blood pressure

108
Q

risk factors and pathophysiolohy of hyperaldosteronism

A

Hypertension, electrolyte imbalance

Excess production of aldosterone
K+ loss, Na incrase, higher blood pressure

109
Q

signs and symptoms of hyperaldosteronism

A

Hypertension
Increased risk of cardiac arrhythmias

Usually asymptomatic
Hypokalaemia - constipation, muscle weakness and cramps, polyuria, polydipsia, paraesthesia
Sweating attacks

110
Q

tests for hyperaldosteronism

A

U and Es - decreased Renin, increased aldosterone

ECG - Rhyme – U have no Pot (K+) and no Tea but a Long PR and a Long QT
There is a long PR nad long QT wave but a flattened T wave on an ECG
This is for CONNS disease!

111
Q

differential diagnosis for hyperaldosteronism

A

Renal artery stenosis
Accelerated hypertension
Diuretics
Congestive HF
Hepatic failure
(these are all causeso fteh secondary type)

112
Q

management for hyperaldosteronism

A

Potaissium s[aring diuretic - spiralactone!
Laproscpoic adrelanectomy to treat cones disease -

113
Q

complications of hyperaldosteronism

A

Chronic high blood pressure

114
Q

what is addisons disease

A

Addisons is an autoimmune condition where there is destrctuion of the adrena cortex leading to deficancies

115
Q

causes of addisons disease, primary and secondary

A
  • Primary
    ○ Addison’s - autoimmune adrenalitis (90% of cases)
    ○ Adrenal TB
    ○ Surgical removal of adrenal glands
    ○ Adrenal haemorrhage/infarction (in meningococcal septicaemia)
    ○ Malignant infiltration – from lung, breast or renal cancer
  • Secondary
    ○ Steroids
    ○ Congenital
    ○ CRH deficiency
    ○ Trauma
    ○ Radiotherapy
116
Q

risk factors for addisons disease

A

Other autoimmune condition ssuch as ovarian faliure, pernicous aneamia, and thyroid disease

117
Q

pathophysiology of addisons disease

A

Autoimmune destructio resulting in reducd to no glucocorticoid and mineral corticoid production
This leads to increase ACTH and CRH
ACTH is what is responsible fo the hyperpigmentation

118
Q

what are the key presintations of addisons

A

TANNED TIRED TONED TEARFUL

119
Q

signs and symptoms of addisosn

A

Postural hypertension
Hyperpigmentation
Virtiligo
Hypoglycaemia

Nausea and vomiting
Abdominal pain
Weight loss
Legarthy
Depression

120
Q

test or addisons

A

ACTH stimulation test - take baseline cortisol, give ACTH (synATCHen) and then remeasure cortisol levels.
Failure of exogenous ACTH to increase plasma cortisol
In Addisons - cortisol remais low after giving ACTH

Plasma ACTH level - high ACTH and low cortisol is primary, low both is secondary

Adrenals CXR

Look for adrenal antibodies

U and Es - high plasma renin and rasied urea shows aldosterone mysfunctions

121
Q

manegment for addisons disease

A

Glucocorticoids - oral hydrocortisone/prednisolone
Mineral corticoids - fludruocortisone to replase aldosterone

Double does of sterioids is needed when unwell, trauma, sugeru and hightwhift work

They should also be given emergancy injection hydrocortisone for adrenal crisis times

122
Q

complications of addisons disease

A

Can present as an emergency (Addisonian crisis) – sudden need for aldosterone and cortisol
* Vomiting + nausea
* Abdominal and back pain
* Muscle cramps
* Confusion
* Hypotension
* Hypoglycaemia
* Hypovolaemic shock
Treat with fluids and IV Hydrocortisone

123
Q

wha are teh commentest causes f addiosns disease bth worldwisde and in teh uk

A

Worldwide = TB
In UK = Addison’s (autoimmune adrenalitis)

124
Q

what is the deforntiiotn of SIADH

A

Continued secretion of ADH despite plasma being very dilute, this causes water retention, excess blood volume and hyponatremia

125
Q

what are teh causes of SIADH

A

alignancy
* Small cell lung carcinoma
* Prostate
* Thymus
* Pancreas
Drugs
* Opiates
* Chlorpropamide
* Carbamexepine
Brian issues:
* Meningitis
* Cerebral abscess
* Head injury
* Tumour

Lung -
* Pneumonia
* TB
* Abscesses
* Asthma
* CF

Metabolic
* Porphyria - body cant process haem
Alcohol withdrawal

126
Q

risk factors for SIADH

A

age >50 years
pulmonary conditions (e.g., pneumonia)
nursing home residence
postoperative state

127
Q

what os teh pathpphysiology of SIADH

A

Excess ADH - causes an insertion of aquaporin 2 and so more water retention

It also decreases the RAAS as there is enough water in the plasma, which means that less aldosterone is release. This means that there is more Na+ secreted which causes hyponatremia!

128
Q

what are teh keypresintation of SIADH

A

Prescence of risk factors
Abscenece of hypovolemia
Absence of hypervolemia
prescence or signs of adreanl insurciacncy ot hypothyroidism

129
Q

what are the signs and symptoms of siadh

A

Concentrated Urine
Hyponatremia

Reduced GCS
Irritability
Headaches
Anorexia
Nausea

130
Q

what are teh first line test for SIADH

A

It needs to be distinguished from hyponatremia, diagnostic criteria:
- Low serum sodium
- Low plasma osmolality
- Inappropriate urine osmolality
- Continued urinary sodium excretion
- Absence of hypokalaemia
- Normal renal, adrenal and thyroid function

  • Test with 1-2L of 0.9% saline – sodium depletion WILL respond, SIADH will NOT
131
Q

what are teh differential diagnoses for SIADH

A

Pseudohyponatraemia due to hyperglycaemia, hyperlipidaemia, or hyperproteinaemia should be ruled out first

Renal failure, adrenal insufficiency, and appropriate release of AVP secondary to extracellular volume depletion (hypovolaemia, due to gastrointestinal or renal loss) or intravascular volume depletion (hypervolaemia due to congestive heart failure, cirrhosis of the liver, or nephrotic syndrome) must be ruled out in order to diagnose SIADH.

132
Q

what is the treatment for SIADH

A

Treat the cause

* Restrict fluid to increase the Na 
* Demecocycline - inhibts vasopression on the kidneys - cuase nephrogenic DI 
* Tolvaptan - treatment og hyponatremai secondary to SIDAH as prmotes water excretion with no loss of electrolytes  Furosemide - salt and loop diruetics help prevent overload
133
Q

what is diabeties insipidus

A

a lack of ADH

134
Q

what is a risk factor for diabeties insipidus

A

sickle cell disease

135
Q

what is teh pathophysiologyy of teh two types of diabeties insipidus

A

Cranial - too little ADH released form the pituitary gland
* Neurosurgery
* Head trauma
* Pituitry disease
* Infiltrative disease
* Idiopathic
* Congenital defect in ADH making gene
Nephrogenic - kidney just not responding to it
* Drugs
* Hypokalemia
* Hypercalceamia
* Sickle cell disease
Familelia - ADH receptor mutation

136
Q

what are teh sympotms of diabeties insipidus

A

Polyuria
Polydipsia
Dehydration

137
Q

what are teh first line tests for diabeties insipidus

A

Water deprivation test - aims to see if the kidneys will still dilute water even if dehydrates
Normal response would be for urine to become concentrated

Desmopressin (ADH analogue) can then be given to see if it is kidney or brain related, if the urine osmolarity remains the same it is nephrogenic, if it changes it is cranial

138
Q

what are teh otehr tests for diabeties insipidus

A
  • MRI of hypothalamous
  • Plasma biochemistry - high or normal Na+
  • Bloog glucose, serum K and Ca2+ should be measured to exclude oyeh causs of polyuria
  • Urine volume ot confirm polyuria
139
Q

differenctial diagnosis for diabeties insipidus

A

Primary polydipsia - drinking too much water

140
Q

what is teh treatment for diabeties insipidus

A

Cranial DI - demopressin
Nephrogenic DI -
○ Bendroflumethiazide (diuretic) – causes more Na+ secretion in DCT 🡪 increased water lost makes body respond by reducing GFR
○ NSAIDs – reduce GFR by inhibiting prostaglandin synthase (prostaglandins locally inhibit ADH action)

Drink a certain amount of water each day

look out for hypnatremia!

141
Q

what are teh three types of hyperpartnyroidism

A

Primary - excessive PTH secretion
Secondary - physiological compensatory hypertrophy of all the glands in response to hypocalcaemia (vit D deficiency, chronic kidney disease)
Tertiary - autonomous parathyroid hyperplasia after long standing secondary hyperparathyroidism, plasma calcium and PTH are raised

142
Q

what are eth risk factors for hyperparathyroidism

A

Genetics, women after menapause, radiation therapy in the neck

143
Q

whatare ethe signs and symptoms of hyperparathyroidms

A

Fractures and osteoporosis hypertension

  • Painful bones,
  • Renal stones,
  • psychiatric moans(legarthy, memory loss, depression, psychciss, insomnia, these are caused by the excess calcium)
  • Abdominal groans - nausea, vomiting, constipation
  • Thirst and polyuria
144
Q

what is the tests for hyperparathyrpidism

A

Blood test for parathyroid horone -
○ Primary - ↑PTH, ↑Ca, ↓Phosphate
○ Secondary - ↑ PTH, ↓ Ca, ↑ Phosphate (due to renal disease)
○ Tertiary - ↑ everything (progression of secondary)

  • Increaaaaaed urinary caliucm excretion
  • Bone scan for density
  • Abdominal xray
  • Radioisotope scanning for detecting adeanomas in the body
145
Q

what is teh treatment for promary hyperparathyroidism

A

Primary
* Parathyroid adenoma- surgical removal
* Remove the parathyroid glands, causes hypocalceamia
* Give calcimeitic (cinacalet) that increases senstitivity of parathyroid cells to Ca2
* Avoid thiazide diuretics and high calcium and vitamin d intake

146
Q

what is teh treatment for secondary and tertary hyperparathyroidm and for emergacnsys?

A

Secondary and tertiary - treat the cause (renal problems)
Emergancy
* rehydrate with 0.9% NaCl
* give biphosphne to preovent bone reabsorbtion y inhibiting the osteoblastasts after rehydration
* Measure serum U and Es daily

147
Q

what are teh causes of hypoparathyroidism

A

Syndromes
Genetic
Surgical
Radiation
Autoimmune
Infiltration
Magnesium deficancy

148
Q

what is teh pathophysiology of hypoparathyroidism

A
  • Autoimmune destruction of parathyroid cland
  • Vitamin D defiecancy causing less Ca2+ can lead to autoimmune destruction?
149
Q

key symptoms of hypoparathyroidism

A

SPASMODICT
Spasms – carpopedal spasms = trousseau’s sign
Perioral paraesthesia (around mouth)
Anxious, irritable, irritational
Seizures
Muscle tone increases
Orientation impaired and confusion
Dermatitis
Impetigo herpetiformis – psoriatic pustules
Chvostek’s sign, cataracts, cardiomyopathy
Trousseaus sign

150
Q

signs and symptoms of hypoparathyroidism

A
  • Chvostek’s sign - involutary twithng of facial misces when the cheek is gently tapped infrot of the ear
  • Convulsiotn
  • Arrhymthia
  • Tetany
  • Trousseau’s sign – carpopedal spasm induced by inflation of the sphygmomanometer cuff to ~20 mmHg above systolic BP
  • Spasms (hands and feet, larynx, premature labour)
  • Periheral paraesthesia
  • Anxiety
  • Seizures
  • Muscle tone increase
151
Q

hypoparathyrpidmsm teste

A

Blood test to measure parathyroid and calcium levels,
phosphate levels will be high,

152
Q

differenctia diagnosis for hypoparathyroidism

A

Type 1 diabetes, Addison’s diseas, ceaoliac disease

153
Q

management for hypoparathyrpidms

A
  • Calcium supplement
  • Calcitriol (active vitamin D)
    Synthetic PTH
154
Q

what is pseudohypoparathyroidism

A
  • There is also pseudohypoparathyroidism!
  • Resistance to PTH hormone due to mutaiton on subunit
  • Bloodworks show low calcium and high PTH
  • Treated as nomeal hypoparathyroidism
  • Associated with short stature, short metacarpals (especially 4th and 5th), subcutaneous calcification and sometimes intellectual impairment
155
Q

what is a pheocrocytoma

A

A tumour in the adrenal gland causing too much adrenaline to be released

156
Q

what is teh aetiology of a pheocromacytoma

A
  • Tumour in the adrenal medulla which cause the release of catecholamines (85% of cases)
  • The other 15% us causes by paragangliomas on the spinal cord which can be due to hereditary syndromes
157
Q

what are the risk factors of pheocromacytoma

A

Having the heredity syndromes endocrine neoplasia type 2 or Von Hippel-Lindau syndrome

Succiate dehydrogenase subunit b c and d gene mutation

158
Q

what are teh key presintations of pheocromacytoma

A

Headache
Palpitations
Diaphoresis - excessive sweating

159
Q

what are teh signs and symptoms of pheocromacytoma

A

Orthostatic hypotension (postureal hypotention)
Hypercalceamia
Cushigns sundrom
Abdminal masses

Diahorrhea
Fever
Tremors

160
Q

what are teh tests for pheocromacytoma

A

24 hour urine collection for catchelocamies, normetaphrrines and creatine

Genetic testing

Palsma catcholocamines

  • serum free metanephrines and normetanephrines

FBC
serum calcium
serum potassium
chromogranin A

161
Q

what are teh differenctial diagnosis for a pheocromacytoma

A

Anxiety, carcinoid syndrome
Hyperthyroidism

162
Q

what is teh treatment for a pheocromacytoma

A

Beta blockers to reduce the effect

Surgery to remove the tumour

163
Q

what are the risk factros for hypercalceamia

A
  • Non metastatic malignancy
  • Metastatic skeletal involvement
  • Lymphoma
    History of malignancy

older age lady

164
Q

causes of hypercalceamia

A

90% of causea are caused by either
* Malignancy
- bone mets, myeloma, PTHrP, lymphoma
* Primary hyperparathyroidism

Other factors:
* Thiazides
* Thyrotoxicosis
* Sarcoidosis
* Familial hypocalciuric / benign hypercalcaemia
* Immobilisation
* Milk-alkali
* Adrenal insufficiency
* Phaeochromocytoma

165
Q

what is teh mneumonic for teh causes of hyercalceamia

A

CHIMPANZEES:

* Calcium supplementation 
* Hyperparathyroidism 
* Iatrogenic drugs (thiazides) 
* Milk alkali syndrome 
* Pagets disease 
* Acromegaly and Addison's 
* Zolinger-ellison syndrome 
* Excess vitamin d 
* Excess vitamin a 
* Sarcoidosis
166
Q

what is teh pathophysiology f hypercalceamia in cancer patients

A

It’s common for cancer patients as it can cause metastasis in kidneys or in bone which causes breakdown and so increased calcium release. This is called hymoural hypercalceamia of malignancy

167
Q

signs and symptoms of hypercalceamia

A

Short QT segment on ECG
Dry mucus membranes
Poor skin turgour

Painful bones-
Renal stones
Psychiatry moans - le

legarthy fatigue, memory loss, psychosis, depression
Abdominal groans - GI symptoms (nausea, constipation, indigestions)
Cardiac arrest!

168
Q

what are the tests for hypercalceamia

A

ECG - tented T, short QT interval

CXR to rule of myeloma and non Hodgkin’s lymphoma
24 hour calcium
Bloods - undetectable PTH excludes primary hyperparathyroidism and requires further investigation
X ray
DEXA bone scan
Hight resolution CT
TSH test to write out hyperthyroidism
synACTHen test for Addison’s - small dose of ACTH is given to test if it will cause a spike in cortisol

169
Q

differential diagnosis for hyperalceamia

A

Adrenal insufficiency, hyperthyroidism, hyperparathyroidism, pheocromcacytoma, pulmonary tuberculosus

Tuberculosis can cause hypercalceamia becuas of the granulomas have lts of macrophages which are able to change the vitamin d inot its active form.

170
Q

managemtn of hypercalceamia

A

Lowering calcium levels and treating the underlyign cause

Primary hyperparthyrpidism - surgical removla of adenoma
IV saline - dilute levels of calium in eh blood
Biphosphenates - encourage osteoclasts to apoptose so there is less bone breakdown (risdronate)

171
Q

complicait of hypercalceaima

A

Acute kidney injury, coma, acute pancreatitis.

172
Q

in hypocalceamia, what three cuases and what are the calcium levels, PTH leves, phosophate levels and id teh PTF appropriate or inaprotriate

A

Disorder PTH Calcium Phosphate PFH
Vit D deficiency Hight low low Appropriate
Hypoparathyroidism low low high Innapropriate
Pseudohypoparathyroidism High low High Appropriae

173
Q

what are the cuases of hypocalceamia

A
  • Vitamin d deficiency - poor calcium uptake and also decreased absorption leads to osteomalacia
    • Acute pancreastitus - the sepsis causes more catchelocomines to be release hihc causes a shift in circulating calcium
    • Osteomalacia - there is less calcium in the bones meaning that there is less to be reabsored which its low
    • Chronic kidney disease - high phosphate levels as well because there is poor uptake of calcium as well and tehre is inadequate vitamin d nd so there is renal phosphate retetntion
    • Pseudohypoparathyroidism- resistance to PTH due to a mutation in the parathyroid gland
    • Drugs - calcitonin, biphsophates reduce the osteoclast activity resulting in reduced Ca2+
      Hypoparathyroidism
174
Q

what are teh signs of hypocalceamia

A
  • It will cause the QT interval on an (ECG) to become longer if there is less calcium in the body
  • Convulsions
  • arrhythmias
  • Chvosteks sign (tapping on the facial nerve causes twitching of face)
  • Trousseaus sign - carpopedal spasm induced by inflated sphygmomanometer cuff

There are the same symptoms as with hypoparathyroidism
Remember the main ones by -

SPASMODICT
* Spasms
* Paraesthesia
* Anxiety
* Seizures
* Muscle tonicity increased
* Orientation impaired and confused
* Impetigo herpeformis
* Chvostek’s sign (face)
* Trousseaus sign (arm)

175
Q

what are teh symptoms of hypocalcaemia

A

Spasms (hands and feet, larynx, premature labour)
Peripheral paraesthesia
Anxiety
Seizures
Muscle tone increase

176
Q

what are the tests for hypocalceamia

A

ECG - long QT interval
Bloods -there will be low calcium and potentially an abnormal phosphate as well

177
Q

what is teh differencial diagnosis for hypocalceamia

A

Iantrogenic postsurgical hypoparathyroidism
Vit d deficiency
Hypo magnesia
Hyperventilation

178
Q

what is teh treatment for hypocalceamia

A

Sever:
* Calcium gluconate - this is calcium salt which increases levels of calcium in the blood and also binds to excess potassium and magnesium in the blood
Mild:
* Adcal supplement (calcium carbonate ) or cholecalciferol (vit d in inactive form)

179
Q

what are teh causes of hyperkaleamia

A

Cramping of smooth muscle, weakness of skeletal and arrhythmias and arrest of cardiac.

Exxessive consumption (IV fluids)

Low levels of aldoseteron n the kidneys causes more to be kept

Drugs - potassium sparing diruetics, nsaids, heparin, ace inhibirots as the block the binding of aldosterone to the receptors

Acute kidney injury - decrased filtration rate

Metanloic acidosis - ketoacidosis,

180
Q

what is teh pathophyisology of hyperkaleamia

A

K levels are controlled by uptake of k into cells, renal excretion and extrarena losses such as GI

The amount in reh blood helps deterine the excitability og the nerve and muscles cells

When levels rise it creates a reduced electrical potentail between cardiac mycocyte and so the action potentail secreases causing arrhythemias and cardiac arrest

In metabolci acidodsis the body tries to compensae by moevinh h+ ions into cells in exchange for K+ into the bloocd which can cause ther hyperkalemia

181
Q

signs and symptoms of hyperkaleamia

A

Metaboicl acidosis causesin kussmauls respiration
Tachycardia

  • Often asymptomatic until high enough to cause cardiac arrets
  • Muscle weakness
  • Impaired neuromuscular transmission
  • Flaccid paralysis
  • Chest pain
  • Light headedness
182
Q

tests for hyperkaleamia

A

U and e - if it is over 6.6mmol/l its hyperkalemia and if its over 6.5mmol/litre it’s a medical emergancy

ECG - small t waves, small p, wide qrs complex

183
Q

manegemnt for hyperkaleamia

A

Moderate - treat underlysing cause, dietry potassium restriction, change of drugs if theyre causing ti, loop diuretic furosemide to increase urinary K+ excretion

Severe -
○ Calcium gluconate – decreases VF risk in the heart and protects myocardium by reducing excitability of cardiac myocytes
○ Insulin and dextrose – drives K+ into the cells
○ Polystyrene sulphonate resin – binds K+ in the gut decreasing uptake

184
Q

what is pseudohyperkalemia

A

It could be pseudohyperkalemia where the blood test causes tehre to be excess levels of k in te hblood due to thke clentching their fist to get the blood, or heamolysis

185
Q

defornition of hypokalemia

A

Low potassium level in the body below serum <3.5mmol, severe is <2.5mmol

186
Q

causes of hypokaleamia

A

Fasting, anorexia,

high levels of aldosterone n the kidneys ( Cushing’s and conns) increased renal excretion (loop diuretics and thiazide diuretics), GI losses

GI causes - Vomiting, severe diahorhea, laxative abuse

187
Q

pathophysiology of hypokaleamia

A

Low k+ in the serum causes a water concentration gradient out of the cell

Increased leakage from the ICF causing hyperpolarisation of the monocyte membrane decreasing the excitability which causes

188
Q

symptoms of hypokaleamia

A

Usually asymptomatic - muscle weakness, cramps, tetany (muscle spasms), palpitation, constipation

189
Q

test for hypokaelamia

A

U and E’s - <3.5 is hypokalaemia <2.5 is a medical emergency!!!

ECG :
* U waves
* Depressed ST segment
* Small or inverted T
* Lond PR
* Long QT

There is a rhyme - ‘have no POT (K+), have no Tea, but a long PR and a long QT

190
Q

differencial diagnosis for hypokaleamia

A

Vomiting
Severe diarrhoea
Laxative and bowel cleansing agent use
Bulimia nervosa

191
Q

treatment for hypokaleamia

A

Mild - oral K+ and spironolactone - K+ sparing diuretic
Severe - IV K+

192
Q

defien hypernatreamia

A

Plasma sodium >145mmol

193
Q

pidemiology and risk factors for hypernatreaima

A

Those at either extremes of age and those physically or cognitively debilitated, mortality rates can be quite high for those of greater age

Diabetes (insipidus or mellitus)
Kidney disease

194
Q

causes of hypernatreamia

A

Normally form water loss
Hyperosmolar hyperglycaemic state caused by badly managed diabetes
sodium gain
Mineralocorticoid excess
Diabetes insipidus

195
Q

pathophysiology for hypernatreimia

A

The patient will often present hypovolemic state if its due to osmotic diuresis. If its due to diabetes insipidus it will most likely be due to
Because of the high salt in the blood, water from the cells will move into the blood, which can cause lots of neural problems.
If they are hypovolemic

196
Q

mnemumonic for hypernatreiam causes

A

MODEL:
Medication
Osmotic diuresis
Diabetes insipidus
Excessive water loss
Low water intake

197
Q

symptoms of hypernatreiamia

A

Muscle weakness
Restlessness
Thirst
Confusion
Legarthy
Confusion
Seizures
Unconsciousness
Changes in urination
Muscel twitching

198
Q

test for hypernatreiama

A

U and E- Na of >145mmol/l is hypernatremia
Urine osmolarity may help determine the causes - normal respons is highly concentrated very little urine, hypertonic urine suggests extra reanl fluid loss (vomiting diharrohea, burns) isotonic sugests osmotic diuresis, diuretic use and hypotonic suggests diabetes insipidus

Head CT looking for intercranial haemorrhage and brain syrinkage

199
Q

differenital diagnosis dor hypernateriamia

A

Diabetes insipidus
Hyperosmolar hyperglycaemic state
Nephrogenic diabetes insipidus
Severe diahorrhea

200
Q

treatemtn of hypernatreiamia

A

Replace water defect SLOWLY!!!!!!
Wit NaCL 0.9% and glucose 5%
If its given too fast cerebreral oedema will occur

Treat the underlying causes despressin for diabetes insipidus

201
Q

complications of hypernatreeamia

A

Moderate to severe hypernatraemia can cause acute brain shrinkage with vascular rupture, haemorrhage, demyelination and permanent neurological injury
Infants and small children are more vulnerable to hypernatraemia due to greater insensible losses and inability to communicate their need for fluids or access fluids independently

202
Q

define hyponatreamia

A

A serum sodium concentration of less than 135mmol/l, it is the most common electrolyte disorder encountered

203
Q

reik factors for hyponatreiama

A

Old age
Hospitalisation
SSRI use
Thiazide diuretic use

204
Q

causes of hyponatreamia

A

Normally caused by an increase in renal water intake due to ADH (SIADH) the most common causes is hypo-osmolar hyponatraemia.

Hypovolemic:
-GI fluid loss
-Mineralocorticoid deficiency

Hypervolemic:
- Kidney injury and disease
- Congestive heart failure
- Cirrhosis

Euvolemic:
- Medications
- SIADH
- High fluid intake
- Medical testing (cardiac catheterisation)

205
Q

key presintation of hyponatriam

A

presence of risk factors
high fluid intake
fluid losses
history of diabetes mellitus

206
Q

signs and symptoms of hyponatreima

A

Odema, weight changes, absence of auxillery sweat, poor skin turgour

Confusion, headache, balance problems, altered metal stare, low urine output, weught changes,

207
Q

tests for hyponatreamia

A

Serum sodium concentration
serum electrolytes, urea, creatinine, and glucose
serum osmolality
urine sodium concentration
Urine osmolality

CT of the brain, tests to find the underlying cause

208
Q

differential diagnosis for hyponatreamia

A

Chirrosis, heart faliure, kidney faliure, primary polydipsia

209
Q

treatent for hyponatreamia

A

Hypertonic solution of 3% saline over 24 hours

Restrict the fluid intake if euvolemic or hypervolemic
Tolvaptan - (competitive ADH receptor)

210
Q

what is teh synacten test

A

synactes in artifical ACTH

it can help tell if teh adran insurficanc of cortisol is due to teh pituitry or adrenals

if its given and cortisol increases its probably due to the pituitry not working properly

211
Q

what is the Essential criteria for the diagnosis of SIADH

A

Hyponatraemia < 135 mmol/L
Plasma hypo-osmolality < 275 mOsm/Kg
Urine osmolality > 100 mOsm/Kg
Clinical euvolaemia
No clinical signs of hypovolaemia (orthostatic decreases in blood pressure, tachycardia, decreased skin turgor, dry mucous membranes)
No clinical signs of hypervolaemia (oedema, ascites)
Increased urinary sodium excretion > 30 mmol/L with normal salt and water intake
Exclude recent diuretic use, renal disease, hypothyroidism, and hypocortisolism

212
Q

what are the 4 main causes of SIADH

A

central nevous system (head inury, brain lesion, infection)
tumours
respiratory causes (pnumonia, TB, asthma, pnumothorx)
drugs - ssris, carbamazapine, vasopressin, demopressin, chloroproramide.

213
Q

where is leptin secreted from

A

white adipose tissue

214
Q

what is teh treatment for hyponatramia

A

mild or asymptomatic - fluid restriction

severe - 3% saline

215
Q

if a patient with addisons presents with a chest infection what should you do

A

double teh steroid dose as teh body normally produces more steroid whne under stress

216
Q

where is grenlin released from

A

the stomach

217
Q

what is teh gold standard test for acromegally

A
  • Oral glucose tolerance test
    ○ Normally a rise in blood glucose will suppress GH levels
    Give glucose and then test GH levels – if they remain high this is diagnostic for acromegaly
218
Q

why do you not do GH test or acromegally

A

GH is released in pulses and so isnt very accurate.

219
Q

who should you not give carbimazole to and what should they be give instead

A

pregnant ladies

propylthiouracil

220
Q

what is a dangerous side effects of carbimazole you need to tell teh patient about

A
221
Q

what is a dangerous side effects of carbimazole you need to tell teh patient about

A

antigranulosis - a deficany of granulocytes in teh blood, causing inceased vunrability to infection as it depresses teh bone marrow

tell teh patiensts tat if they get any signs of infection they need to stop taking it e.g a sore throat

222
Q

why does alchholism causes hypoparathyroidism

A

alcohol is a magnesuim diuretic and cuases teh magnesium to leave the body. This leads to low Mg levels. Mg is needed to make parathyroid hormone, so this leads to hypoparathyroidism and hypocalceamia

223
Q

what are two effects of insulin on cells whihc doesnt include glucose

A

drived [otassium into teh cells

surpresses growth hormone

224
Q

what medication would uou give to some who is pregncnt with graves hyperthyroidism

A

PROPYLTHIOURACIL - carbimazole is teatrogenic

Phase 2a (18 decks)

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