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Jay-Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

When the blood glucose levels decrease, what cells detect the change? What do they release as a result of this change?

A

Alpha cells in the Islets of Langerhans.

Glucagon

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2
Q

When the blood glucose levels increase, what cells detect the change? What do they release as a result of this change?

A

Beta cells in the Islets of Langerhans.

Insulin

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3
Q

Insulin release is stimulated by what type of neurons?

A

Parasympathetic

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4
Q

Briefly describe what Type 1 diabetes is?

A

An autoimmune disease causing destruction of beta cells leading to insulin deficiency. Caused by genetic and environmental triggers

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5
Q

In type 1 diabetes, insulin isn’t secreted. What is the chain of effect on the body?

A

Continued breakdown of liver glycogen to blood glucose. Unrestrained lipolysis and muscle breakdown. Glucose is not up taken.

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6
Q

What are the common symptoms and causes of a presenting Type 1 diabetic?

A 
Polyuria- excessive passing of urine
Polydipsia- extreme thirst
Weight loss- body in catabolic state
Glycosuria- excess glucose in urine
Ketonuria- ketones present in urine
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7
Q

Explain the pathophysiology of ketone formation in uncontrolled type 1 diabetes

A

Lack of insulin leads to increased glucagon levels
Leads to an increased catabolic state. Fat breakdown produces more FFA and glycerol. FFA provide energy oxidised into ketone bodies –> ketoacidosis

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8
Q

What is the main treatment for type 1 diabetes?

A

Insulin therapy

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9
Q

What is the name of the type of T1 diabetes presenting later in life with a slower insulin dependence?

A

Latent autoimmune diabetes of adults (LADA)

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10
Q

Name some non-modifiable risk factors of type 2 diabetes

A

Older age
Men
Asian ethnicity

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11
Q

Briefly describe the pathophysiology of type 2 diabetes

A

Either impaired insulin secretion or insulin resistance –>
Impaired glucose tolerance- higher than normal levels glucose –> progressive hyperglycaemia and high FFA –> reduced muscle and fat uptake after eating + reduced lipolysis and high FFA –> glycosuria (high sugar in urine).

Still v low levels of insulin protects from muscle catabolism so v rarely get ketonuria

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12
Q

Name the modifiable risk factors of type 2 diabetes mellitus

A 
Obesity
Calorie excess/ bad diet
Lack of exercise
Smoking
Alcohol consumption
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13
Q

What are some indications of pre-diabetes?

A

Impaired glucose tolerance- high blood glucose levels

Impaired fasting glucose

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14
Q

What is a good test used to look at longer term blood glucose?

A

HbA1c- glycated haemoglobin

A type of haemoglobin with glucose attached. Gives long term view of blood glucose levels.

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15
Q

For the HbA1c test- what level is classed as normal, pre-diabetic and diabetic? (units value and %)

A

Normal: <39 / <5.7%
Pre-diabetes: 39-46 / 6.4%
Diabetes: >46 / >6.4%

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16
Q

What are three commonly used drug treatments for T2 diabetes and how do they work?

A

Metformin (oral)- increase insulin sensitivity. SE: diarrhoea, nausea.
Sulfonylurea (oral)- increase insulin secretion. SE: hypoglycaemia, weight gain
Insulin (SC)

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17
Q

What is ketoacidosis and when can it occur?

A

Formation of ketones. Lack of insulin/insensitive –> break down of muscle releasing FFA which are metabolised for energy making ketones.
Can occur in T1 diabetes and starvation.

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18
Q

How would ketoacidosis be diagnosed?

A

Acidaemia- blood pH >7.3
Hyperglycaemia
Ketonemia- ketones in urine

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19
Q

What are some potential complications of ketoacidosis?

A

Cerebral oedema, aspiration pneumonia, hypokalaemia, hypomagnesaemia, hypophosphatemia,
thromboembolism.

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20
Q

What would pre-dispose somebody to have a hyperosmolar hyperglycaemic non ketotic coma

A

Type 2 diabetic

Dehydrated with high glucose. No acidosis

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21
Q

Name some common complications of type 2 diabetes

A 
Infections at insulin injection sites
Vascular disease: MI, stroke, hypertension
Nephropathy
Diabetic feet
Ulcerations
Cataracts
Diabetic retinopathy
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22
Q

What is the commonest presentation of thyroid disease?

A

Goitre- a swelling of the thyroid gland causing a lump on the front of the neck

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23
Q

What is the function of thyroid hormone?

A 
Develops the NS
Metabolic rate
Breathing and HR
F or F response
Regulation of vital body functions: e.g body weight, cholesterol levels, body temp etc
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24
Q

Briefly describe what Graves disease is

A

An autoimmune disease of the thyroid.

Most common cause of hyperthyroidism by overproducing thyroid hormones. 2/3rds of hyperthyroid cases due to it

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25
Q

What are some signs and symptoms of Graves disease?

A 
Irritability
Weight loss
Muscle weakness
Sleeping problems
Tachycardia
Heat intolerance
Diarrhoea
Graves opthalmothapy- bulging eyes
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26
Q

What is the treatment for Graves disease?

A

Anti-thyroid drugs
Thyroidectomy- removal of all or part of thyroid
Methyl prednisolone

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27
Q

What is thyrotoxicosis?

A

An excess of thyroid hormone in the body from ANY CAUSE

Therefore also low level of TSH (thyroid stimulating hormone)

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28
Q

Define hyperthyroidism

A

An overactive thyroid gland leading to an excess of thyroid hormone levels

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29
Q

What can cause hyperthyroidism?

A

Graves disease
Adenoma- benign tumour of glandular tissue causing increased release
Congenital
Drug induced: Iodine, amiodarone (treats arrhythmias but can prevent T3 to T4 conversion, lithium

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30
Q

What are some common symptoms of hyperthyroidism?

A 
Weight loss
Goitre
Tachycardia
Palpitations
Hyperphagia- increased appetite
Anxiety
Tremor
Irritable
Heat intolerance and sweating- in shorts in winter etc
etc
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31
Q

What are the common signs (not symptoms) of hyperthyroidism?

A

Graves: goitre, eye disease

Adenoma- solitary nodules

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32
Q

What investigations are done for suspected hyperthyroidism?

A

Thyroid function test- increased T3 and T4. Elevated TSH in primary, suppressed in secondary.
Diagnose/find underlying cause
Antibodies
Isotope uptake scan

33
Q

What is the difference between primary and secondary hypertension?

A

Primary- where the pathology is in the thyroid gland

Secondary- resulting from elevated TSH in circulation

34
Q

What hormone controls the release of thyroid hormone in the thyroid gland and where is it made?

A

Thyroid stimulating hormone (TSH). Made in anterior pituitary gland

35
Q

What is the treatment for hyperthyroidism?

A

Anti-thyroid drugs- Carbimazole or methimazole- prevents new synthesis of thyroid hormone
Radio-iodine
Surgery

36
Q

Name another autoimmune cause of hyperthyroidism caused by an antibody-mediated response causing primary hyperthyroidism.

A

Hashimoto’s thyroiditis

37
Q

What’s the name of the condition where there’s reduced levels of thyroid hormone in the body

A

Hypothyroidism

38
Q

What’s the most common cause of hypothyroidism?

A

Iodine deficiency

39
Q

What are the common symptoms of hypothyroidism?

A 
Tiredness/ sleepy/ lethargic
Decreased mood
Cold dislike- probably very wrapped up
Weight loss
Constipation
Menorrhagia- heavy periods
Hoarse voice 
Decreased cognitive ability
40
Q

What are some common signs (not symptoms) of hypothyroidism?

A 
BRADYCARDIC- acronym
B
R- reflexes relax slowly
A- ataxia (cerebellar)coordination, balance and speech
D- dry, thin skin and hair
Y- yawning
C- cold hands- +/- temp
A- ascites +/- non-pitting oedema +/- pericardial effusion
R- round puffy face/obese
D- defeated demeanour
I- immobile +/- ileus (immobile bowel)
C- CCF (congestive cardiac failure)

Also: neuropathy, myopathy, goitre

41
Q

How do you diagnose hypothyroidism?

A

Inreased TSH, T4 decrease
Cholesterol and triglyceride increase
Macrocytosis- enlarged RBC

42
Q

How would you test for thyroid malignancy?

A 
Hard nodule on neck- swollen lymph glands, hoarse voice, dysphagia (swallowing difficulties)
Blood test- hyperthyroidism
\+ Thyroid function test
Ultrasound
Biopsy
43
Q

What are the treatments available for thyroid cancer?

A

Radioactive iodine- thyroid cancers take up iodine so radioactive can destroy these cells. (Chemo and radio therapy doesn’t work)
Thyroxine- suppresses TSH
Surgery

44
Q

Where is parathyroid secreted from?

A

One of four parathyroid glands located posterior to the thyroid

45
Q

What stimulates the release of parathyroid hormone?

A

Secreted in response to low Ca2+ levels in the blood. A -ve feedback loop

46
Q

What affect does parathyroid hormone have around the body?

A

Increased osteoclast activity- releases more Ca(2+) and PO4(3-) from bones
Increases reabsorption of Ca2+ in kidneys
Decreases reabsorption of PO4(3-)Active 1,25 dihydroxy-vitamin D3 production is increased- causes increased Ca2+ and decreased PO43-

47
Q

What are the main cause of primary hyperparathyroidism?

A

Solitary adenoma- 80%
Hyperplasia of all glands- 20%
<0.5% parathyroid cancer
Loss of feedback

48
Q

How would hyperparathyroidism present?

A

Often asymptomatic
Increased Ca2+ can cause: weak, tired, depressed, thirsty, dehydrated but polyureic, renal stones, abdo pain, pancreatitis, ulcers.
Bone reabsorption- pain, fractures, osteoporosis
Increased BP- check Ca2+ in patients with hypertension

49
Q

How would you test for hyperparathyroidism?

A

Increased Ca2+ and PTH
Decreased PO4(3-)
Bone imaging
DEXA- for osteoporosis

50
Q

What is the difference between primary, secondary and tertiary hyperparathyroidism?

A

Primary- hypercalcaemia results from abnormally active parathyroid gland e.g. an adenoma in gland
Secondary- hypocalcaemia caused by a response to a lack of Ca2+ in the blood, reactive overproduction of PTH, cause not due to parathyroid gland pathology. E.g. decreased vit D intake, chronic kidney failure
Tertiary- hypercalcaemia develops from prolonged untreated secondary, elevated PTH. Seen in chronic kidney failure

51
Q

What is hypoparathyroidism and what is the main cause?

A

Decreased PTH secretion due to parathyroid gland failure.

52
Q

What are the main causes of primary hypoparathyroidism?

A

Autoimmune condition, congenital (from birth)- Di George syndrome

53
Q

What are the causes of secondary hypoparathyroidism?

A

Radiation
Surgery- thyroidectomy, parathyroidectomy
Hypomagnesaemia- magnesium is required for PTH secretion

54
Q

What is the pathophysiology of pseudohypoparathyroidism? And what are the symptoms/signs?

A

Failure of target cell response to PTH
Signs: Short metacarpals (4th and 5th more often), round face, short stature, calcified basal ganglia, decreased iQ.
Treatment: same as for primary- Ca2+ supplements and calcitriol (an active form of vit D)

55
Q

What is the treatment for primary hypoparathyroidism?

A

Calcium supplements

Calcitriol- an active from of vit D

56
Q

Name the types of steroids made in the adrenal cortex

A

Glucocorticoids- e.g. cortisol. Affects carbohydrate, lipid and protein metabolism Mineralocorticoids- e.g. aldosterone. Control sodium and potassium balance
Adrenal androgens- sex hormones that are converted peripherally into testosterone and dihydrotestosterone

57
Q

What type of hormone is cortisol and where is it made in the body?

A

Glucocorticoid steroid hormone.

Made and released from the adrenal cortex

58
Q

Name an example of a mineralocorticoid steroid hormone and it’s function in the body.

A

Aldosterone. Increases sodium (and water) reabsorption in the kidney in exchange for potassium and hydrogen ions. Very involved in the RAAS system to control blood pressure.

59
Q

What is the mechanism/cause behind Cushing’s Syndrome? What’s it’s most common cause and symptoms?

A

Chronic cortisol excess
Cause: most commonly due to oral steroids. Sometimes due to benign overactive tumour.
Symptoms: Weight gain/more body fat centrally and on chest and neck (Buffalo Hump). Puffy red face.

60
Q

What hormone regulates the level of cortisol in the body?

A

ACTH- adrenocorticotropic hormone

61
Q

What is the pathophysiology of Conn’s syndrome?

A

Excess production of aldosterone- leads to having more Na+ and H2O retention, more K+ excreted, decreased renin released

62
Q

What are the potential causes of Conn’s Syndrome?

A

Adenoma in renal tissue-

63
Q

What are the symptoms and their pathophysiology of Conn’s disease?

A

High blood pressure- too much aldosterone –> Na+ and water retention, K+ excretion –> hypokalaemia –> muscle dysfunction and heart arrhythmias!

64
Q

What are two potential pathological causes and treatments of Conn’s syndrome?

A

Unilateral adenoma in renal tissue- remove one gland so removing problematic adenoma so reduced aldosterone made
Bilateral adrenal hyperplasia- can’t remove as will cause Addison’s. So give Spironolactone drug (an aldosterone antagonist)

65
Q

Describe what Acromegaly is and its cause

A

Caused by the abnormal excess secretion of Growth Hormone in adults. 99% caused by hyperplasia

66
Q

What are the symptoms of acromegaly?

A 
Acroparaesthesia- tingling/numbness/pain in extremities after sleep
Amenorrhoea- missed periods
Decreased libido
Headache
Increased sweating
Snoring
Arthralgia- joint pain
Backache
67
Q

What are the signs of acromegaly?

A 
Increased growth in hands, feet and jaw
Coarsening face, wide nose, big tongue, widely spaced teeth, puffy lips, eyelids and skin
Obstructive sleep apnoea
Goitre
Proximal weakness and pain
Carpal tunnel signs in 50%
68
Q

What are some complications of acromegaly?

A

Impaired glucose tolerance
Diabetes mellitus
Vascular: BP increase, left ventricular hypertrophy, cardiomyopathy, IHD, stroke, neoplasia: colon cancer risk

69
Q

What is a Prolactinoma

A

Adenoma of the pituitary gland causes overproduction of prolactin. Causes reduction in sex hormone production

70
Q

What are the symptoms/signs of a prolactinoma?

What treatment is used?

A

Local effect of tumour: headache, visual field defects, CSF leak
Effects of increased prolactin levels: amenorrhoea or irregular periods, infertility, galactorrhoea (Xs breast milk production).
Treatment: dopamine agonists

71
Q

Adrenal insufficiency is also known as….?

What’s the main causes (in the UK and worldwide)?

A 
Addison's Disease
Main cause in UK: Autoimmunity- 80%
Globally: TB
Other causes: adrenal metastases e.g. from lung, breast or renal cancer. Lymphoma
Opportunistic infections in HIV
Adrenal haemorrhage
Congenital
72
Q

What are the symptoms of adrenal deficiency/Addison’s disease?

A

Late diagnosis: lean, tanned, tired, tearful, anorexia, dizzy, faints
Mood: depression, psychosis, low self-esteem
GI: nausea/vomiting, abdo pain, diarrhoea/constipation
*think of Addison’s in unexplained abdo pain +/- vomiting

73
Q

What test results/findings would be indicate Addison’s disease?

A

Bloods
Lack of mineralocorticoid (mainly aldosterone) leads to decreased Na+ and increased K+
Glucose decreased- due to decreased cortisol
Uraemia- urea in blood
Increased Ca2+
Eosinophilia- high levels of eosinophils
Anaemia

74
Q

What treatment would you give to a patient with Addison’s disease?

A

Replace steroids- hydrocortisone

Mineralocorticoids replacement

75
Q

Describe the condition Diabetes insipidus

A

Passage of large vols of water due to impaired resorption in the kidney caused by either reduced ADH secretion from posterior pituitary (cranial) or impaired response in kidney to ADH (nephrogenic) Excessive thirst and excessive weeing of dilute urine

76
Q

What are some potential causes of diabetes insipidus?

A

Electrolyte imbalance (hypercalcaemia, hypokalaemia)
Kidney disease
Chronic lithium ingestion
Genetic

77
Q

What are the symptoms of diabetes insipidus?

A

Polyuria- excessive urination
Polydipsia- excessive thirst
Dehydration
Symptoms of hypernatremia- v high Na+ in blood

78
Q

What are the two types of diabetes insipidus? What are their treatments options?

A

Cranial DI- hypothalamus doesn’t produce enough ADH.
Test and Treatment: MRI head to find cause. Give desmopressin- synthetic ADH
Nephrogenic DI- kidneys fail to respond to ADH. Treat cause

Jay-Phase 2a (3 decks)

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