3D Endocrine

Question 1

How does insulin work?

Answer 1

Insulin regulates glucose levels in the bloodstream and induces glucose storage in the liver, muscles, and adipose tissue, resulting in overall weight gain.

Insulin opens glucose channels - ‘pushes’ the glucose from the blood into the cells -> Reduces blood sugar

Question 2

Types of diabetes?

In type 1 diabetes c-peptide is ____
In type 2 diabetes c-peptide is ____

Answer 2

In type 1 diabetes c-peptide is LOW
In type 2 diabetes c-peptide is HIGH

To clarify between type 1 and 2 diabetes if unsure, NICE guidelines suggest testing of C-peptide. This peptide is the result of the cleavage of proinsulin into insulin. Very low levels indicate the absolute absence of insulin, indicating type 1 diabetes mellitus.

Question 3

Fasting glucose
- Normal
- Diabetic

Random glucose / after food
- Normal
- Diabetic

Normal HBA1c?
Pre-diabetic?
Diabetic HBA1C?

Answer 3

Fasting glucose
- Normal <6.1
- Diabetic >7.0

Random/after food glcose
- Normal < 7.8
- Diabetic > 11.1

Impaired fasting glucose

HBA1C
- Normal <42
- Pre-diabetic 43-47
- Diabetic >48 (6.5%)
- Diabetics prone to hypos 53 (7%)

Question 4

Aetiology of type 1 diabetes?
Aetiology of type 2 diabetes?

Answer 4

1 - Absolute insulin deficiency secondary to T-cell mediated autoimmune destruction of the insulin producing B cells

Question 5

What drugs are given for T2DM
1st line
2nd line (obese)
2nd line (not obese)

Answer 5

Order

(Lifestyle changes first)

1st line - . Biguanideas - Metformin 500mg. Insulin sensitiser. Liver - decreases gluconeogenesis.= in muscle and liver. Weight neutral/loss.
SE: diarrhoea (take with a meal to reduce SE), lactic acidosis. Caution in renal failure.
X AKI - have to stop
Stop metformin if eGFR <30.

2nd line - depends on renal function, cardiovascular disease, weight, occupation (eg. lorry driver wont want insulin).
If obese SGKT2 or GLP1.

2nd line- SGLT2 inhibitor - sodium glucose channel inhibitor. Inhibits glucose reabsorption in kidneys. Increased excretion of glucose in urine.
Dapa/empagliflozin. (-gliflozin)
Diuresis. Calorie loss - weight loss.
SE: Lots of UTI, euglycaemic DKA in T2DM, fourniere’s gangrene.

2nd line - GLP1 receptor agonist - increase glucagon/insulin secretion, increase satiety, slow gastric emptying. Liraglutide. Tablet or injection? RESTRICTED due to cost/availabilty ‘weight loss drug’. More likely to get if co-morbid eg sleep apnoea, BMI > 35.

If not obese sulphonyurea or insulin.

2nd line (not obese) Sulphonylureas - Gliclazide 80mg. Blocks ATP sensitive potassium channels → exocytosis of stored insulin. 3/4th line. Can cause hypos and weight gain.

3rd DPP4 inhibitors - Sitagliptin. (-gliptin) SE: Pancreatitis **3rd line after metformin, SGLT2, if HBA1C not controlled. Weight neutral. No risk of hypo.

3rd Thiazolidinediones - Pioglitazone. Reduces insulin resistance. SE: oedema, fluid retention. CI: HF, Bladder Ca.
__________________________________________
LESS COMMON

3rd Meglitinides- Repaglinide 1mg.

3rd Alpha glucosidase inhibitors- Acarbose 25mg. Prevents absorption of glucose.

Question 6

What type of insulin for:
- Type 1 diabetes
- Type 2 diabetes

Answer 6

Insulin for type 1 - insulin pump OR basal bolus regime (base line plus boluses with meals TDS).
Check blood glucose QDS.

Insulin for type 2 - long or intermediate acting to start with.
Check blood glucose less.

Question 7

Diabetes yearly check, what is involved?
Foot exam - what signs appear first?

Answer 7

BP, Cholesterol, BMI
Urine - albumin/creatinine ratio (nephropathy)
Eye (retinopathy)
Neuropathy (peripheral and autonomic)
Feet - first signs :
1. Decreased vibration sense
2. Reduced/absent ankle jerk reflex

Question 8

What cells in the pancreas produce the insulin?

Answer 8

Beta cells

Question 9

DKA
-Usually found in what type of diabetes?
- BG?
- Blood ketone?
- pH?

Answer 9

Type 1 Diabetes (autoimmune) (or end stage/long term Type 2)- high BG
New diagnosis - replace volume deficit. Usually dehydrated.

BG > 11 mmol
Blood ketone >/ 3.0 mmol or ++ in urine
pH < 7.30 and/or HCO3 < 15.0 (mol/L)

Question 10

HHS (Hyperosmolar hyperglycaemic state)

Cause?
Difference to DKA?
What are the 4 principle treatments for HHS?

Answer 10

Cause - insulin pump deficiency, T2DM, steroid induced diabetes.

Type 2 diabetes (insulin resistance)- high BG
Takes longer to build up than DKA, BG is higher.

Hyperglycaemia BG >30 mmol/L
Hyperosmolality >320 mosmol/kg (osmolality - Na+Na+ Glucose+urea)
Hypovolaemia >7L -ve fluid balance

X No significant ketosis. Blood ketone <3.0 mmol/L
X No significant metabolic acidosis. pH>7.30, HCO3>15.0

HHS4 - fluid, monitoring, FRIII (not always necessary, if so half dose of infusion for DKA), treat underlying causes eg. chest infection.

Question 11

DKA symptoms
Treatment?

Answer 11

Metabolic acidosis
Can be caused by SGLT2 inhibitors (don’t take when unwell - sick day rules)

Nocturia, polyuria, thirsty, dehydration, tired and unwell, weight loss. Nausea, vomiting, breathless, ketotic breath, abdominal pain, confused and drowsy → coma.

Treatment
- replace fluids
- fixed rate insulin infusion
- monitoring (fluid balance, blood gas, ketones, hourly BG) Caution with heart/renal/liver failure. K monitoring.

SICK DAY RULES - insulin requirement INCREASES if unwell. DON’T STOP insulin.
Whereas metformin STOP when unwell to avoid AKI.

Question 12

Macrovascular and microvascular complications of diabetes?

Answer 12

Question 13

What are the exocrine functions of the pancreas?
and endocrine function?

Answer 13

Exocrine - produces enzymes to digest food in the small intestine (eg. amylase, lipase, trypsin, chymotripsin)

Endocrine - produces hormones (insulin and glucagon) to regulate blood sugar levels

Long version:

Exocrine function: The pancreas produces enzymes that help to digest food in the small intestine. These enzymes include amylase, which breaks down carbohydrates; lipase, which breaks down fats; and trypsin and chymotrypsin, which breaks down proteins. The process of pancreatic secretion involves chemical work and is linked to an increase in the amount of oxygen that is consumed. The pancreatic duct cells contain carbonic anhydrase, which allows them to produce the hydrogen carbonate that is then expelled into the duct lumen.

Endocrine function: The pancreas also produces hormones, including insulin and glucagon, which help to regulate blood sugar levels. Insulin promotes the uptake of glucose into cells, while glucagon promotes the release of glucose from the liver.
Overall the pancreas plays a vital role in maintaining the body’s metabolism and energy balance.

Question 14

1. The release of thyroid hormones is regulated by the _______________, which secretes __________________.
2. Thyroid stores what mineral?
3. What hormones are stored in the thyroid gland?

Answer 14

1. The release of thyroid hormones ( Fig. 3.1 ) is regulated by the anterior pituitary gland, which secretes thyroid-stimulating hormone (TSH).
2. Iodine
3. Three hormones are synthesized and secreted in the thyroid gland:

• Thyroxine (T 4 )
• Tri-iodothyronine (T 3 )
• Calcitonin (involved in calcium homeostasis)

Fig. 3.1
Hormonal regulation of the thyroid hormones. (T 3 , tri-iodothyronine; T 4 , thyroxine; TRH, thyrotrophin-releasing hormone; TSH, thyroid-stimulating hormone.)

Question 15

Hypothyroidism
- Symptoms?
- Blood test results (primary hypothyroidism, secondary hypothyroidism)
- Causes

Answer 15

Hypothyroidism is the deficient release of thyroid hormone resulting in an abnormally low metabolism.

Symptoms
- Feeling lethargic
- Feeling cold
- Unexplained weight gain
- Goiter (swelling)

Blood results, Primary hypothyroidism (issue is thyroid gland)
-T3/4 low
-TSH high
Secondary hypothyroidism (issue is pituitary gland)
- T3/4 low
- TSH low

Causes
- Autoimmune
- Surgery
- Viral
- Tumour
- Drug induced (eg treatment for hyperthyroidism carbimazole, propylthiouracil, lithium
- Radiation
- Trauma
- Congenital (heel prick test)
- Peripheral hypothyroidism - gene mutation, resistance to thyroid hormones. Hormone is produced but not able to work.

Question 16

Hyperthyroidism
- Symptoms?
- Causes?

Answer 16

Hyperthyroidism is the excessive release of thyroid hormones resulting in an abnormally raised metabolism.

Symptoms
- Hot
- Sweaty
- Unexplained weight loss

Causes
The main causes of hyperthyroidism are:

• Graves’ disease – an autoimmune disease
• Toxic mulitnodular goitre – nodules develop that secrete thyroid hormones, most commonly seen in elderly patients and in populations where iodine intake is too low.
• Toxic adenoma – a benign growth that secretes T 3 and T 4 .
  Additional (and rarer) causes include subacute (de Quervain’s) thyroiditis, ectopic thyroid tissue, drugs, e.g. amiodarone or thyroxine, overdose.

Question 17

Hyperthyroidism
- How is it diagnosed?
- Treatment?

Answer 17

Thyroid function tests -
Thyroid function tests are the main method of diagnosis. Serum TSH, free T 3 and free T 4 are measured by radioimmunoassay (RIA). Elevated T 3 and T 4 levels indicate hyperthyroidism is present. Raised TSH suggests the fault lies in or above the pituitary gland, whereas low TSH points to a thyroid organ disorder.

Other tests include:

• Autoantibody screening, e.g. Graves’ disease
• Radioisotope scanning to show the size of the thyroid gland and any abnormal ‘hot’ areas such as a toxic adenoma
• ECG to check for sinus tachycardia or atrial fibrillation (as a result of excess thyroid hormones).

Treatment
Treatment varies depending on the cause of the hyperthyroidism and requires specialist monitoring and control in infancy and pregnancy. The main treatments, however, can be divided into three methods:

1. Drug therapy: β-blockers for rapid symptomatic control, e.g. palpitations, anxiety. Carbimazole inhibits the peroxidase reactions of T 3 and T 4 synthesis but can take around a month to have a marked effect. Some physicians use a block–replace method, i.e. treat with carbimazole and thyroxine simultaneously to avoid risk of iatrogenic hypothyroidism.
2. Radioiodine ( 131 I) : 131 I is only absorbed by the thyroid tissue, killing the cells and reducing thyroid hormone synthesis. The response is slow and carbimazole may still be required.
3. Partial thyroidectomy: The thyroid gland is removed surgically leaving some tissue and the parathyroid glands.
   Both radioiodine and partial thyroidectomy run the risk of long-term hypothyroidism as the remaining thyroid tissue may not be sufficient to meet the body’s demands, especially with increasing age. Their treatment is described under hypothyroidism.

Question 18

Graves disease
- What is the cause?
- Symptoms
- Tests / Diagnosis

Answer 18

Cause - autoimmune disease, in which autoantibodies against the TSH receptors are produced. These antibodies stimulate the TSH receptors and lead to an excess production of thyroid hormones.
-Can be iodine induced (amiodarone has high levels of iodine)

Autoantibodies to thyroglobulin and to the thyroid hormones may also be produced. Graves’ disease is the most common cause of hyperthyroidism and thyrotoxicosis; and is especially common in middle-aged women (♀:♂, 8:1). There is a genetic association with the human leucocyte antigen (HLA).

The disease itself follows either a relapsing–remitting course or one with fluctuating severity. Graves’ can lead to hypothyroidism in some rare cases.

SYMPTOMS - Classically, Graves’ disease presents with a ‘staring’ appearance (exophthalmos), a goitre (with bruit) and swollen legs (pretibial myxoedema).

Graves’ ophthalmopathy is caused by lymphocytic infiltration of the periorbital tissues and activation of fibroblasts to secrete osmotically active hyaluronic acid. This increases the pressure and pushes the eye forward, resulting in proptosis. This pressure change also causes muscle fibrosis and diplopia due to weakening of the extraocular muscles. Corneal ulcers are also important to be aware of and inflammation can cause optic nerve compression. The eye disease may precede the onset of thyroid dysfunction, and does not respond to correction of thyroid status. Treatment involves radiotherapy and surgery.

Graves’ disease is diagnosed by detection of autoantibodies along with low TSH and raised T 4 and/or T 3 . The thyroid autoantibodies, thyroglobulin antibody (TgAb) and thyroid peroxidase (TPO) antibody, are present in both Graves’ disease and Hashimoto’s thyroiditis. However, thyroid receptor antibody (TRAb) or thyroid-stimulating hormone receptor (TSH-R) antibodies are specific to Graves’ disease. The treatment is consistent with other causes of hyperthyroidism, but radioactive iodine and surgery are especially likely to cause hypothyroidism.

Question 19

Pituitary gland
- what hormones are released by the posterior lobe, and by what mechanism?
- what hormones are released by the anterior lobe, and by what mechanism?

Answer 19

Posterior (neural)
- Oxytocin
- ADH (anti-diuretic hormone)
Posterior pituitary gland cannot produce its own hormones, it just stores and releases them. Not true endocrine gland.

Anterior (hormonal - hypophyseal portal system)
Acronym : Go Look For The Adenoma Please!
- GH (growth hormone)
- LH
- FSH
- TSH (thyroid stimulating hormone)
- ACTH (adrenocorticotropic hormone)
- Prolactin

Question 20

Hypothalamus produces and releases which hormone?

Answer 20

TRH - Thyrotropin releasing hormone
PRH - Prolactin releasing hormone
GnRH - Gonadotopin releasing hormone (→ FSH/LH)
CRT - Corticotropin releasing hormone
GHRH - Growth hormone releasing hormone

Question 21

Describe the hypothalamic-pituitary-gonodal (HPG) axis
- Hormone released by hypothalamus?
- Hormone released by pituitary gland?
- Target organs?
- Function

Answer 21

GnRH
LH
Ovaries & Testes
Stimulates oestrogen and testosterone synthesis

Question 22

Describe the hypothalamic-pituitary-thyroid (HPT) axis
- Hormone released by hypothalamus?
- Hormone released by pituitary gland?
- Target organs?
- Function

Answer 22

TRH
TSH
Thyroid gland
Stimulate thyroxine synthesis

Question 23

Describe the hypothalamic-pituitary-adrenal (HPA) axis
- Hormone released by hypothalamus?
- Hormone released by pituitary gland?
- Target organs?
- Function

Answer 23

CRH (corticotropin releasing hormone)
ACTH (adrenocorticotropic hormone) AKA Corticotropin
Adrenal cortex
Stimulate corticosteroid synthesis → cortisol is made

The central role of the HPA axis is to modulate the response to stress, culminating in the release of cortisol - a key mediator in a number of metabolic responses and controlled via feedback

Question 24

Cortisol
- Type of molecule?
- Released by?
- What time of day is it highest and best to check?
- Name of the test to check?

Answer 24

Glucocorticoid
Adrenal gland (on top of kidney)

Cortisol is a steroid hormone that is produced by your 2 adrenal glands, which sit on top of each kidney. When you are stressed, increased cortisol is released into your bloodstream.

Highest in morning, Check 9am.

The short synacthen test is one of the commonest tests used to check cortisol function. With the short synacthen test, the adrenal gland is stimulated by an injection of a drug (synacthen), which is chemically similar to ACTH.

Question 25

Blood tests for hypothyroidism? - Primary - Secondary - Subclinical

Answer 25

Primary - Low T3/4, High TSH Secondary - Low T3/4, low TSH Hyperthyroidism (treated) - Normal/high T4, low TSH Subclinical hypothyroidism - Normal T3/4, High TSH. Treat only if pregnant.

Question 26

Adrenal insufficiency

Answer 26

Adrenal gland not producing enough cortisol. Can be confused with hypothyroidism - cause adrenal crisis Replace steroids first before starting thyroxine, to avoid adrenal crisis

Question 27

Blood tests for hyperthyroidism

Answer 27

High T3/4 Low TSH

Question 28

Causes of hyperthyroidism. Mostcommon?

Answer 28

Graves - easy to diagnose Other causes - not as easy. Thyroid uptake scan.

Question 29

Symptoms of a thyroid storm?

Answer 29

Question 30

Treatment for hyperthyroid

Answer 30

Carbimzole 20mg BD Propylthiouracil (PTU) 200mg BD - best for pregnant patients.

Question 31

Metabolic syndrome diagnostic criteria?

Answer 31

Question 32

Pancreas - what is - Behind it - In front - Medial -Lateral

Answer 32

Behind pancreas: Aorta In front of pancreas: stomach Medial to pancreas: Duodenum Lateral to pancreas: spleen

Question 33

Thyroid anatomy - what nerve is superior to thyroid - what nerve is inferior to thyroid

Answer 33

External laryngeal nerve Recurrent laryngeal nerve

Question 34

Suggest 3-5 situations where HBA1C is not to be used and why?

Answer 34

- Pregnancy (haemodiliution) - Children (turnover too high) - Anaemia (unreliable) - If HBA1C done within last 3 months (no point as will get the same result) - Onset of symptoms in the last few months (would not be enough time to show a result)

Question 35

What is the mechanism of action of - Metformin - SGLT2 inhibitor

Answer 35

Metformin - insulin sensitiser SGLT2 inhibitor - glucose excretor

Question 36

Diabetic eye changes What are the signs of - Background diabetic retinopathy - Pre-proliferative retinopathy - Proliferative retinopathy

Answer 36

Question 37

What drugs are given for hyperthyroidism? Name three side effects

Answer 37

Question 38

Name three distinctive symptoms of Graves's disease

Answer 38

Question 39

Actions of insulin, after meal? Fasting state, what happens?

Answer 39

Question 40

Layers of the adrenal gland - Give example hormones for each layer RAA Mineralocorticoid HPA Glucocorticoid HPA Sex hormones SNS Catecholamines

Question 41

Aldosterone function

Answer 41

Reabsorbs sodium from urine, water comes with it, therefore reduce BP? Measured by barometers in juxtaglomerular apparatus Production of renin decreased

Question 42

Addisonian crisis Tests?

Answer 42

Acute deficiency of cortisol Addisonian crisis, also known as adrenal crisis or acute adrenal insufficiency, is an endocrinologic emergency with a high mortality rate secondary to physiologic derangements from an acute deficiency of the adrenal hormone cortisol, requiring immediate recognition and treatment to avoid death Tests - Na, K, cortisol, aldosterone, ACTH (adrenocorticotrophic hormone) Not all adrenal insufficiency is Addisons - Adrenal insufficiency can be primary (adrenal cortex) - Addison's (autoimmune), TB, AIDS, metastatic cancer or secondary

Question 43

Phaeochromocytoma Where in kidney? Symptoms?

Answer 43

Medulla Hypertension (will be resistant to treatment with BP tablets) Think exam stress - sweaty, tachy, feeling anxious etc. A phaeochromocytoma is a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline. In patients with a phaeochromocytoma, the adrenaline tends to be secreted in bursts, giving intermittent symptoms. 24 hr urine collection - HIAA (acid) https://zerotofinals.com/medicine/endocrinology/phaeochromocytoma/

Question 44

What is a thyroid storm? Symptoms? Causes? Emergency treatment?

Answer 44

Thyroid storm (also called thyroid crisis and thyrotoxic crisis) happens when your thyroid gland releases a large amount of thyroid hormone in a short amount of time. It’s a rare complication of hyperthyroidism. Thyroid storm is a medical emergency and is life-threatening. Sudden events that can trigger a thyroid storm include: - Suddenly stop taking your antithyroid medication. - Thyroid surgery (thyroidectomy). - Nonthyroid surgery. - Trauma. - Infection. - Acute illnesses such as diabetic ketoacidosis (DKA), heart failure and a drug reaction. - A sudden large amount of iodine in your body, such as from an iodinated contrast agent that’s used for certain imaging procedures. Hydrocortisone 200mg IM - self pen. oral wont work. Go to hospital → IV steroids.

Question 45

What are the steps of the thyroid examination

Answer 45

Hands - temp, nails - clubbing, palmar thickening, pulse, tremor (paper) Head - hair thinning, pallor, puffiness, proptosis (look from side and looking up), lid retraction, eye movements and lid lag Thyroid + lymph node - Palpation, tongue out, swallow. Percuss thymus Arm movement Shins - pre-tibial myxoedema

Question 46

Thyroid history - questions to ask

Answer 46

Any problems with drinking /swallowing Lump in neck Changes in eye appearance Cold/hot Brady/tachycardia Pyrexia Confusion / cognitive impairment Weight loss / gain Headache Change in vision Hair loss Change in energy levels

Question 47

Prescribing Carbimazole Levothyroxine

Question 48

1. Cushings disease? 2. Cushing syndrome? How to diagnose Cushing's syndrome?

Answer 48

1. Pituitary Tumour caused by too much ACTH? 2. Often caused by doctor giving too much steroid Diagnosis -24hr urinary free cortisol x2 - Low dose dexamethasone suppression test See slide

Question 49

Answer 49

1. Primary hypothyroidism (problem in thyroid) 2. Primary hyperthyroidism (problem in thyroid) 3. Secondary / tertiary hypothyridism (problem in pituitary gland /hypothalamus) 4. Secondary / tertiary (problem in pituitary / hypothalamus) hyperthyroidism 5. Euthyroid sick syndrome (ESS) refers to abnormal thyroid levels – resulting from an acute illness – in a patient with no preexisting or current dysfunction in the thyroid gland. ESS is also known as nonthyroidal illness syndrome (NTIS), sick euthyroid syndrome (SES), Thats why you shouldn't usually measure thyroid levels in a sick patient

Question 50

Anterior pituitary - 6 hormones? Posterior pituitary - 2 key hormones? Which ones are under positive feedback

Answer 50

Anterior - GH, ACTH, TSH, FSH, LH, Prolactin Posterior - Oxytocin and ADH Positive feedback - prolactin and oxytocin. The rest are under negative feedback.

Question 51

Effects of low levels of each pituitary hormone (hypopituitarism)

Answer 51

Question 52

What level of prolactin indicates prolactinoma? What drugs affect prolactin levels?

Answer 52

figure in 5/6 digits is definite prolactinoma Anti-emetic eg, Metaclopramide, and anti-psychotics. Check prolactin before starting these drugs.

Question 53

Short synacthen test, what gland does it check? Insulin stress test. Get BG down to what level?

Answer 53

Adrenal gland 2.2

Question 54

What is a non-functioning pituitary tumour? Types of functioning tumours? Most common?

Answer 54

Doesn't produce its own hormones. Functioning tumours - Prolactinoma (most common) - Acromegaly - Cushing's - TSHoma - GNoma (gonadotrophinoma)

Question 55

Cushing's disease - how to diagnose?

Answer 55

Question 56

Never suspend desmopressin Sick day rules for steroids

Answer 56

Double steroid dose when sick

Question 57

What is leptin? What is ghrelin? Where is is released from? When?

Answer 57

Leptin - senses satiety. Hormone that lives in our fat tissue, goes to hypothalamus, tells us we're not hungry. Leptin level is stable an rarely changes. No leptin = keep on eating, get fat. Ghrelin - senses hunger. Sensation of hunger - Key players, ghrelin (orexigenic - appetite stimulant) Driven by ghrelin, which is released from stomach during fasting in direct response to reduced stretch of the stomach, thus firing off the mechanoreceptors. Ghrelin acts at the arcuate nucleus to inhibit and stimulate the neurons which respectively serve both the satiety and hunger centres. Levels of ghrelin fall within approximately an hour of food intake. In addition to the direct action of Ghrelin on the arcuate nucleus, information is sent via the vagus nerve from the machanoreceptors of the stomach (sensing no stretch) to the nucleus tractus solitarii (NTS), which in turn triggers inhibition and stimulation at the arcuate nucleus of the corresponding centres.

Question 58

Where is the hunger centre? Where is the satiety centre?

Answer 58

Lateral hypothalamus. Ventromedial nucleus of hypothalamus

Question 59

What substances are released to control hunger and from where?

Answer 59

Question 60

Adenoma's are usually rich in what?

Answer 60

Lipids

Question 61

What does this CT scan show? What do alpha cells produce? What do beta cells produce? D cells? F cells?

Answer 61

Normal pancreas Glucagon Insulin

Question 62

Ultrasound assessment of thyroid nodules, what does the classification U1 mean? U5?

Answer 62

U1 - Normal U2 - Benign U3 - Indeterminate U4 - Suspicious U5 - Malignant Black centre = good. Not malignant. Grey centre = bad. Suspicious for malignancy.

Question 63

Adrenal gland What hormones are released by each zone? Give examples

Answer 63

Question 64

In females: 1. Where is LH released from? 2. Where is FSH released from? In males 3. Where is LH released from? 4. Where is FSH released from? and what are all the actions

Answer 64

1. Theca cells 2. Granulosa cells 3. Leydig cells 4. Sertoli cells

Question 65

Kallman's syndrome? Sheehan's syndrome

Answer 65

Anosmia, hypopituitarism, gynaecomastia Postpartum hypopituitarism, often due to PPH

Question 66

Addison's - autoimmune Signs & symptoms

Answer 66

Adrenal glands not producing cortisol Skin pigmentation Fatigue Weight loss Postural hypotension Abdo pain / diarrhoea

Question 67

Adrenal insufficiency - investigations?

Answer 67

Random cortisol Short synacthen test - 8/9am (check cortisol, give synthetic acth, recheck cortisol after 1 hour) Adrenal antibodies - to check for Addison's see image + coeliac antibodies

Question 68

Adrenal insufficiency - acute management? Long term management?

Answer 68

IV hydrocortisone 100mg stat is the updated guideline (or 200 is ok) Long term management - 4mg/day prednisolone

Question 69

What is pituitary apoplexy?

Answer 69

Infarction of pituitary gland due to haemorrhage or ischaemia

Question 70

Thyroid storm - Causes - Symptoms - Treatments

Answer 70

Treatment - carbimazole, prednisolone, lithium, propanolol

Question 71

Hypercalcaemia - Most common 2 causes

Answer 71

Most common 2 causes: Primary hyperparathyroidism Malignancy

Question 72

Hypocalcaemia - Signs - Emergency treatment

Answer 72

Sign's - Chvostek's sign - Trousseau's sign Emergency treatment - IV calcium

Question 73

Diabetes insipidus aka deficiency/resistance of what?

Answer 73

Desmopressin Treatment - Hydration. oral/NG water, 5% dextrose. - Desmopressin - Careful monitoring

Question 74

Primary vs secondary vs tertiary hyperparathyroidism

Answer 74

Secondary - Vit D deficient Tertiary - usually malignant transformation of parathyroid glands

Question 75

Normal PTH level Functions of PTH?

Answer 75

Normal PTH < 6 Activates 1 alpha hydroxylate, which converts Vit D from one form to the active form

Question 76

Indications for surgery (hypercalcaemia)

Answer 76

>2.85 calcium → definitely needs surgery parathyroidectomy or 2.6-2.85 with end organ damage or Has osteoporosis Consider if fit enough for surgery/GA. usually short GA, or daycase/LA may be possible

Question 77

Dexamethasone suppression test: what result would indicate - Cushings syndrome - Cushings disease

Answer 77

Cushings syndrome - (too much cortisol) Cushing's disease - (pituitary adenoma) See image

Question 78

What conditions are these tests for? and what are the symptoms of the conditions? 1. Plasma aldosterone/renin ratio 2. Short synacthen test 3. Dexamethasone suppression test

Answer 78

1. Primary hyperaldosteronism (HIGH BP + LOW K) 2. Adrenal insufficiency (LOW BP and LOW Na) 3. Adrenal gland function / Cushing's disease

Question 79

Types of hormones - three classes and give examples of each

Answer 79

Peptide - insulin, glucagon, prolactin, ACTH Steroid - are lipids w/ ring system. Classes: glucocorticoids (prednisolone, cortisol), mineralocorticoids (aldosterone), sex hormones (oestrogen, progesterone, testosterone). eg. cholesterol, all the above Amino acid derivatives - adrenaline, thyroxine

Question 80

Zones of adrenal gland layers

Answer 80

Adrenal gland Way to remember zones , outer to inner - GFR Zona glomerulosa Zona fasciculata Zona reticularis Medulla (inner)

Question 81

Stages of thyroid exam - name as Many steps as you can

Answer 81

https://geekymedics.com/thyroid-status-examination/ Introduction Wash your hands and don PPE if appropriate Introduce yourself to the patient including your name and role Confirm the patient's name and date of birth Briefly explain what the examination will involve using patient-friendly language Gain consent to proceed with the examination Ask the patient to sit on a chair for the assessment Adequately expose the patient’s neck and upper sternum Ask if the patient has any pain before proceeding Gather equipment General inspection Inspect the patient whilst at rest, looking for clinical signs suggestive of underlying pathology Hands Palpate the patient’s radial pulse assessing rate and rhythm Face Inspect the patient’s face for clinical signs suggestive of thyroid pathology (dry skin, excessive sweating, eyebrow loss) Inspect the patient's eyes for evidence of lid retraction, inflammation and exophthalmos Assess for eye movement abnormalities Assess for lid lag Thyroid inspection Inspect the midline of the neck for evidence of thyroid enlargement, lumps or scars Ask the patient to swallow some water and repeat inspection Ask the patient to protrude their tongue and repeat inspection Thyroid palpation Palpate the patient's thyroid gland assessing size, symmetry and consistency. Also note any masses present in the thyroid tissue. Ask the patient to swallow some water whilst you feel for symmetrical elevation of the thyroid lobes Ask the patient to protrude their tongue whilst you palpate Lymph node palpation Palpate local lymph nodes to assess for lymphadenopathy Trachea Inspect for tracheal deviation Percussion of the sternum Percuss downwards from the sternal notch for evidence of retrosternal dullness Auscultation of the thyroid gland Auscultate each lobe of the thyroid for a bruit Special tests Assess biceps reflex Inspect for pretibial myxoedema Ask the patient to stand with their arms crossed to assess for proximal myopathy To complete the examination… Explain to the patient that the examination is now finished Thank the patient for their time Dispose of PPE appropriately and wash your hands Summarise your findings Suggest further assessments and investigations (e.g. thyroid function tests, ECG, ultrasound scan) Total: 0 / 33

Question 82

Cranial nerve examination

Answer 82

https://geekymedics.com/cranial-nerve-exam/

Question 83

Normal values for - Na - K - Urea - Creatinine

Answer 83

Question 84

HHS - what does it stand for? What are the 4 principle treatments for HHS?

Answer 84

HHS4 - fluid - monitoring - FRIII (not always necessary, if so half dose of infusion for DKA) - Treat underlying causes eg. chest infection.

Question 85

Sick day rules for diabetics - General advice - What meds to stop and why? - What med to never stop?

Answer 85

SICK DAY RULES - Drink extra fluids Monitor blood glucose more often Check urine for ketones if you have the sticks Weigh self daily to monitor for dehydration. Call Dr if > 5lb loss. Whereas metformin STOP when unwell to avoid AKI. SGLT2 inhibitor STOP to avoid dehydration / ketones / DKA Insulin requirement INCREASES if unwell. DON'T STOP insulin.

Question 86

DD of neck lump?

Answer 86

Thyroid goitre Thyroid cancer Lymphoma Thyroglossal cysts - painless, moves with swallowing and sticking tongue out. Central? Branchial cysts - Unilateral. Congenital abnormality.

Question 87

Antibody associated with Graves disease?

Answer 87

TSH (thyroid stimulating hormone) Receptor antibodies

Question 88

Low cortisol - primary adrenal insufficiency - name? Cause? - Secondary adrenal insufficiency

Answer 88

Addison's disease - damaged adrenal glands Lack of adrenal stimulation from ACTH - damaged pituitary

Question 89

Dexamethason suppression test 1. Used in what illness? 2. What does it detect? 3. Low dose test: dose, normal result, abnormal result 4. high dose test: dose, results?

Answer 89

1. Cushings 2. If cortisol is suppressed by dexamethasone 3. 1mg Low (suppressed) cortisol = normal. High/normal cortisol = Cushing's syndrome 4. 8mg Low cortisol = Cushing's disease See picture

Question 90

What is Cushing's DISEASE?

Answer 90

Cushing's disease (i.e. pituitary adenoma → ACTH secretion)

Question 91

DIABETES DRUGS - which do/don't cause hypos? - which do/don't cause weight gain?

Answer 91

DPP-4 inhibitors eg. sitagliptin. (Inhibits GLP-1) - no weight gain (weight neutral) - no hypos Sulphonyurea eg. gliclazide - YES weight gain - YES hypos Insulin - YES weight gain - YES hypos Metformin - No weight gain (causes weight loss) - No hypos? GLP-1 (glucagon-like peptide-1) eg. liraglutide, eventide (SC injections). Causes rise in insulin production by pancreas, reduce gastric emptying, decrease appetite. - No weight gain (causes weight loss) - SE: nausea and vomiting Thiazolidinediones eg. pioglitazone - YES weight gain

Question 92

Adrenal crisis Na High/Low? K High/Low?

Answer 92

Addison's disease = primary adrenal insufficiency Adrenal crisis = LOW Na, HIGH K

Question 93

Dexamethasone suppression test. Causes? 1. Cortisol : not suppressed, ACTH : suppressed 2. Cortisol : suppressed, ACTH : suppressed (BOTH SUPPRESSED) 3. Cortisol : not suppressed, ACTH : not suppressed (BOTH NOT SUPPRESSED)

Answer 93