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Medicine Year 3 > Academic Week 4 > Flashcards

Academic Week 4 Flashcards

1
Q

What are the precipitating factors for a DKA or HHS?

A

Inadequate insulin therapy, infection, new onset diabetes, metabolic stressors (surgery/emotions), glucocorticoids, antipsychotics and excess diuretics.

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2
Q

How should pituitary micro-adenomas be treated?

A

These are slow growing and only require observation

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3
Q

How should pituitary macro-adenomas be treated?

A

These are known for their locally invasive properties but distant metastases are very rare. They may require surgical intervention.

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4
Q

What is the difference between Cushing’s disease and Cushing’s syndrome?

A

Cushing’s disease originates in the pituitary with excess ACTH secretion whereas Cushing’s syndrome is the symptoms of cortisol excess.

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5
Q

How does hypopituitism present?

A

GH deficiency, gonadotrophin deficiency, ACTH deficiency, TSH deficiency or vasopressin deficiency.

This should be tested with dynamic hormone measurements such as TSH stimulation tests, GnRH stimulation or glucagon test.

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6
Q

How should pituitary hyper function be assessed such as Cushing’s disease?

A

Dexamethasone suppression test for Cushing’s

Oral glucose testing with GH measurement is also an option

MRI is the preferred choice of imaging

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7
Q

How does hyperprolactinemia present?

A

This presents with amenorrhoea and galactorrhea. They will have suppressed LH and FSH with elevated prolactin levels.

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8
Q

What are the causes of hyperprolactinemia?

A

Hypothyroidism, PCOS, pituitary stalk compression or pituitary masses.

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9
Q

How does Cushing’s disease/syndrome present?

A

Type 2 diabetes, weight gain, easy bruising, hypertension and excess cortisol of blood tests.

Dexamethasone suppression test is used to determine whether it is Cushing’s syndrome or disease.

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10
Q

What are the characteristics of acromegaly?

A

Macroglossia, enlarged facial shape, tall stature and cardiac abnormalities.

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11
Q

How are prolactinomas treated medically?

A

Bromocriptine and cabergoline which are dopamine agonists as this inhibits prolactin

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12
Q

How is acromegaly treated medically?

A

Somatostatin analogs (octreotide) and pegvisomant

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13
Q

How is Cushing’s disease treated medically?

A

Ketoconazole, metyrapine and mitotane

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14
Q

How does multiple endocrine neoplasia type 1 present? (MEN1)

A

Parathyroid tumours (95%), enteropancreatic tumours and anterior pituitary tumours. These patients almost always present with hypoparathyroidism and possibly incidentilomas

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15
Q

Describe follicular adenomas of the thyroid?

A

On histopathology follicular adenomas show compression and fibrotic changes in the thyroid around the tumour capsule. This is a well circumscribed tumour and is non-invasive.

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16
Q

Describe the features of thyroid follicular carcinomas?

A

These are less circumscribed than follicular adenomas, which show vascular invasion. These typically metastasise to the bones, lungs and lymph nodes. The tumour resembles thyroid follicles and distant metastases occur in 20%.

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17
Q

Describe the features of thyroid papillary carcinomas?

A

Histologically they have a papillary architecture with characteristic nuclear changes. Size determines the treatment and mortality.

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18
Q

Describe the features of thyroid medullary carcinomas?

A

These are endocrine carcinomas derived from C cells (which produce calcitonin). It is caused by activating mutations in the RET oncogene. 20% are linked with MEN2A or 2B. These can be stained for calcitonin to prove it is medullary.

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19
Q

Describe the feature of thyroid anaplastic carcinomas?

A

These are the result of de-differentiation and aggressive transformation of a follicular or papillary carcinomas. It is p53 mutation associated and they are very aggressive.

All anaplastic tumours are staged at T4 regardless of size.

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20
Q

How do thyroid neoplasms present?

A

They usually present as solitary nodules. Most solitary thyroid nodules are non-neoplastic, inflammatory or hyperplasia related.

Younger men are more likely to have malignancy thyroid nodules.

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21
Q

What is the treatment for malignant thyroid nodules?

A

Surgery followed by radio iodine ablation of the remaining tissue.

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22
Q

How are malignant thyroid nodules diagnosed and scored?

A

Fine needle aspiration is used to diagnose solitary and malignant nodules and cytology is scored using the Thy scoring system.

If TSH is normal or high then FNA is strongly recommended whereas if it is low then a scan is needed.

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23
Q

Describe the Thy scoring system of thyroid malignancies

A
  1. Non-diagnostic or unsatisfactory (1c is cyst)
  2. All benign lesions
    3a - Neoplasm is possible but unclear
    3f - Neoplasm possible and likely follicular
  3. Suspicious of any malignancy
  4. Malignant

Any Thy score over 3 requires surgery

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24
Q

Describe some long acting insulins

A

Insulin deter (Levemir), glargine (Lantus) and Degludec (Tresiba)

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25
Q

Describe some rapid acting insulins

A

Novorapid (insulin aspart) and Humalog (lispo)

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26
Q

Describe the biochemical properties of insulin

A

Insulin is made of an alpha and a beta polypeptide chain which are joined by two disulphide links. There is a C peptide chain that has no physiological significance and is excreted in urine which allows measurement of endogenous insulin production. Exogenous insulin analogues have small amino acid changes which affects the duration of the injected insulin action.

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27
Q

What is the first line treatment for type 2 diabetes?

A

Lifestyle changes

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28
Q

Describe the mechanism of action, side effects and contraindications for metformin

A

Metformin is a biguanide which is first line pharmacotherapy for T2DM. It inhibits gluconeogenesis and decreases hepatic glucose output.

It also increases insulin mediated glucose utilisation and reduces lipolysis and free fatty acids.

Side effects on nausea, vomiting, bloating and diarrhoea .

Contraindications include renal impairment, liver disease, alcohol excess or lactic acidosis.

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29
Q

Describe some sulphonylureas

A

These directly stimulate insulin secretion from beta cells by binding to ATP-sensitive potassium channels.

The types now used include Gliclazide and glimepiride. They are shorter acting and are renally excreted.

These can be used as a first line treatment or in combination with metformin. They are well tolerated and can be used for patients with CKD. Side effects include hypoglycaemia and weight gain. They are used in MODY.

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30
Q

Describe GLP 1 receptor agonists

A

GLP-1 is produced by L cells in the small intestine and is secreted in response to nutrient intake. Incretin effect is the augmentation of insulin secretion after oral intake of glucose as opposed to intravenous administration of glucose. The incretin effect in patients with T2DM is dramatically reduced and in some cases has stopped. The GLP agonist activate the GLP receptor which causes increased insulin secretion, suppressed glucagon secretion, slower gastric emptying, increases satiety (which leads to weight loss) and beta cell proliferation. Examples include liraglutide, exenatide and dulaglutide.

These are often used for patients with a BMI over 35. Side effects include acute pancreatitis, GI symptoms, headaches, gallbladder disease and can cause DKA if insulin is also being used. They should be avoided in pregnancy and severe hepatic impairment. Liraglutide is contraindicated in gastroparesis, IBD and severe CCF.

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31
Q

Describe Depeptidyl peptidase-4 inhibitors (DPP-4 inhibitors)

A

Examples include sitagliptin, linagliptin and vidagliptin.

DPP-4 is an enzyme expressed on the surface of most cell types. If activated it deactivates various bioactive peptides such as GIP and GLP-1. Its inhibition could potentially affect glucose regulation through higher levels of GLP1 as DPP4 inhibitors block the breakdown of GIP and GLP1. This has a more modest effect than GLP 1 agonists.

It is used as a combination therapy and is usually well tolerated. There is a slight risk of URTI but it does not cause hypoglycaemic events or weight gain. Linagliptin can be used in patients with an eGFR below 30.

32
Q

Describe Thiazolinediones or Glitazones

A

These increase insulin sensitivity by acting on adipose, muscle, and the liver to increase glucose utilisation and decrease glucose production. They bind to and activate peroxisome proliferator-activated receptors which regulate gene expression in response to ligand binding. Therefore there is increased insulin sensitivity, changes in fat metabolism and reduction in free fatty acids.
These can only be used as a combination therapy. It causes fluid retention, weight gain, increased risk of bladder cancer and MI, fractures and hepatotoxicity. They must not be use din patients with heart failure, a history of bladder cancer, active liver disease, type 1 diabetes or in those who are pregnant.

Examples include pioglitazone and rosiglitazone.

33
Q

Describe SGLT2 inhibitors

A

The sodium-glucose co-transporter 2 is present in the proximal tubules and are targeted by an inhibitor which reduces blood glucose by increasing urinary excretion of glucose. These can only be used as an add on. Examples include empagliflozin, canagliflozin and dapaglifozin.

Adverse effects include UTIs, thrush, pyelonephritis and Fournier’s gangrene. AKI, bladder cancer and DKA are other contraindicated. They should be avoided in patients with T1DM, recurrent UTIs, low bone density, foot ulcerations and predisposing risks to DKA.

34
Q

What are the symptoms of hypothyroidism?

A

Fatigue, lethargy, weakness, cold intolerance, mental slowness, depression, constipation, muscle cramps, irregular menses, infertility, mild weight gain, fluid retention and hoarseness.

35
Q

What are the signs of hypothyroidism?

A

Goitre, bradycardia, non-pitting oedema, delayed relaxation, hypertension, slow speech, slow movements and hoarse voice.

36
Q

What are the causes of hypothyroidism?

A

Autoimmune thyroiditis (Hashimoto’s), atrophic (elderly), iodine 131 treatment and pituitary insufficiency.

37
Q

How should hypothyroidism be investigated?

A

TFT blood tests that show high TSH with low T3 and T4 shows hypothyroidism. Antibody checks should also be done.

38
Q

How is hypothyroidism treated?

A

Levothyroxine (T4) is sued which titrates the T4 level to normalise function. This will also provide symptomatic relief.

39
Q

What is Myxoedema?

A

This is a severe hypothyroidism events which presents with non-pitting oedema, dry waxy skin and myxoedema coma.

Myxoedema coma presents with bradycardia, slow speech, incredibly low T4, altered mental status, coma, seizures, hypothermia, respiratory failure, retention and hypoglycaemia.

40
Q

How should myxoedema be treated?

A

Rewarming, correcting, blood pressure, ventilation if needed, broad spectrum antibiotics, hydrocortisone and IV T3/T4 for three days.

41
Q

What are the symptoms of hyperthyroidism?

A

Weight loss, sympathetic overactivity, goitre, thyroid eye signs (Grave’s), toxic adenomas and multi nodular goitres.

42
Q

How should thyrotoxicosis be treated medically?

A

Anti-thyroid medications such as Carbimazole and initial symptomatic relief with beta blockers.

43
Q

How can thyrotoxicosis be managed surgically?

A

This should be offered if there has been a relapse or medication has failed.

Subtotal or total thyroidectomy are the main options. The administration of radio iodine is also used to kill the remaining tissue. This causes hypothyroidism and hence they will develop hypothyroidism and so thyroid hormone replacement therapy will be needed.

44
Q

What are the symptoms of a thyroid storm?

A

Anxiety, restlessness, agitation, psychosis, confusion, coma, thyrotoxic myopathies, tachycardia, AF, chronic heart failure, diarrhoea, vomiting and severe weight loss.

45
Q

How should a thyroid storm be treated?

A

Beta blockade with ABCDE approach as airway management may be needed. Fluid resuscitation may be required and dexamethasone or Lugol’s iodine are also needed for this acute presentation.

46
Q

What diseases are seen in adrenal hyper function?

A

Cushing’s syndrome, conn’s syndrome and androgenisation with adrenal adenomas.

47
Q

What are the causes of adrenal insufficiency?

A

Major psychological stress, bilateral adrenal haemorrhage and sepsis.

Secondary and tertiary causes include pituitary disease but this is less common because of the RAAS system offering some protection.

Exogenous glucorticoids are another major cause.

48
Q

What are the main causes of Cushing’s syndrome?

A

Cushing’s disease is the main cause but 25% are caused by adrenal disease and 10% ectopic causes such as small cell lung cancer or an ACTH producing tumour.

Iatrogenic causes such as steroids in Asthma, RA, and palliative care may also be responsible.

There is a higher incidence in people with diabetes, hypertension, obesity and osteoporosis.

49
Q

What is pseudocushing’s disease?

A

This is seen in patients with chronic severe anxiety/depression, prolonged excess alcohol consumption, obesity, poorly controlled diabetes and HIV infection.

50
Q

How is the dexamethasone test carried out?

A

The Dexamethasone suppression test uses an overnight low dose and cortisol is measured the next morning. If cortisol is low (<50nmol/L) then this is normal. If it is high (>50nmol/L) then further investigations are needed. This involves localising any lesions. If pituitary in origin then trans-sphenoidal microsurgery can be considered or radiotherapy. Cushing’s causes worse vascular disease and thus carriers a risk of prognosis.

51
Q

What is the FISH genetic test?

A

This is used in paediatric cardiology to assess for Di George Syndrome and in Microarrays. Di George is a deletion of chromosome 22q11.2. Microarray is a chromosomal test which is first line for babies with chromosomal abnormalities or intellectual disability. This is a genome wide test and so incidental findings may occur.

52
Q

When is rapid aneuploidy testing done?

A

This is done with amniocentesis for chromosomal trisomy such as 13 (patau), 18 (Edwards) and 21 (Down’s)

53
Q

When should moles (nevi) be investigated?

A

New moles after the age of 40 are unusual and should be investigated. Dysplastic nevi are more likely to develop into melanomas. These are flat, larger and have irregular borders.

54
Q

What types of benign nevus are there?

A

Freckles are benign melanocystic lesions seen in fair haired people.

Dark macules are seen in older people after sun exposure.

Speckled nevi are congenital.

Halo nevi are autoimmune reactions to moles.

Blue nevi and split nevi are other common benign conditions usually seen in children.

55
Q

Describe the characteristics of melanoma

A

Melanomas are malignant neoplasms of the melanocytes which affects people of all ages but carries a significant mortality in younger people.

They are treatable if excised properly. The prognosis depends on the depth of invasion. Advanced melanoma will be treated with targeted therapies and immunotherapies.

Clinical features are asymmetry, border, colour, diameter and elevation.

56
Q

What are the benign differentials for melanoma?

A

Seborrhoeic keratosis, dermatofibroma or vascular lesions.

Vascular lesions include campbell de Morgan spots, haemongioma, spider angioma, and pyogenic granuloma.

Some epidermoid cysts have a black puncta which are mistaken for large blackheads.

Other malignant differentials are pigmented BCC.

57
Q

Describe basal cell carcinomas

A

BCCs can be subdivided into nodular, superficial, infiltrative (morphoeic) and pigmented. Risk factors include chronic UV exposure (rather than burning), immunosuppression, fair skin, genetic and sites of chronic inflammation or scars. Nodular BCCs have rolled edges, crusting ulceration with central depression, pearly appearance and telangiectasia. Scabbing and healing on a repeated basis makes a lesion suspicious of cancer.

Treatment is with excision, Mohs micrographic surgery or radiotherapy. For a superficial BCC curettage, photodynamic therapy and imiquimod cream, which is 80% effective, are used.

58
Q

Describe squamous cell carcinomas

A

Excision is usually curative but radiotherapy may be needed. Metastases are unusual. Clinically these look like raised spots with a keratin growth in the middle.

Pre-cancerous lesions: There is no precursor to BCC but actinic keratoses are precancerous for SCC. These are rough keratin patches which do not itch. This is treated with cryotherapy, curettage, Efudix, photodynamic therapy, imiquimod and diclofenac gel.

Bowen’s disease often presents as discrete lesion on the legs which are asymptomatic. Treatment is similar to actinic keratoses. This need treatment because it can be an SCC in situ and should therefore be removed.

59
Q

Describe impetigo

A

Impetigo almost always occurs in children and is caused by streptococcus pyogenes (group A strep) or staphylococcus aureus.

It should be throughly cleaned and the child should be kept away from others temporarily. First line treatment is hydrogenperoxide cream or oral antibiotics such as flucoxicillin or erythromycin.

60
Q

How should infected eczema be treated?

A

This is also likely to have been caused by Strep P or Staph A and should only be treated if problematic with topical fusibet or oral flucoxicillin. MRSA may be responsible in resistant lesions.

61
Q

What is folliculitis and how is it treated?

A

This does not normally need treatment unless it is problematic. Then clindamycin may be required. Chronic folliculitis is treated like acne with lymecycline.

62
Q

How does cellulitis present and how is it treated?

A

Cellulitis presents with shiny, swollen, erythematous lesions with a clear border and are unilateral. A portal of entry should be assessed such as an ulcer. This is treated with systemic antibiotics and this is normally caused by strep organisms. Erysipelas is a streptococcal variant of cellulitis which needs penicillin treatment.

63
Q

What is staphylococcal scalded skin syndrome?

A

Staphylococcal scalded skin syndrome (SSSS) is toxic mediated by a small area of previous infection which has not been effectively treated. It is extremely painful. These patients need admitting, analgesia, antibiotics and greasy lotion.

64
Q

What do HSV 1 and HSV 2 cause?

A

HSV type 1 causes cold sores, usually around the mouth. This often has a prodrome of pain in the lip and so treatment with topical acyclovir can prevent it developing. The initial skin lesion is a vesicle which rapidly break down and weep. Then the crusting occurs which is the cold sore. In HIV cold sores can be very problematic.

HSV type 2 causes genital warts.

Golden crusting lesions on the face which may have vesicles, have secondary impetiginisation, punctate, scabbed, discrete lesions with coalescence. Eczema hepeticum, caused by HSV, has a mortality rate associated with it. This is treated with acyclovir. There will have been a sudden deterioration in eczema and can produce erythema multiforme.

65
Q

Describe chickenpox

A

Chickenpox presents with a vesicles surrounded by erythema. It is caused by varicella zoster virus. This is very itchy so the child will scratch the vesicle off. It is transmitted by respiratory droplets and incubates for around 14 days. It is contagious from 2 days prior to 5 days after the onset of the rash. In adults it can be more severe and in immunosuppression it can even cause hepatitis, encephalitis and pneumonitis.

66
Q

Describe shingles

A

Shingles presents with vesicles and crusting in a dermatomal distribution. This means it never crosses the midline. This is caused by reactivation of the varicella zoster virus. This normal affects the elderly. Chickenpox lies normal in the dorsal root ganglion and if reactivated it can cause ophthalmic problems, Ramsey Hunt Syndrome, post hepatic neuralgia, encephalitis and secondary bacterial infections.

67
Q

Describe Molluscum Contagiosum

A

Molluscum Contagiosum presents with umbillicated papules with a shiny appearance, usually in the young, and there will be a lot of them. It commonly occurs with eczema. It is caused by molluscipox virus. This is usually self limiting but it can be curetted off or treated with cryotherapy.

68
Q

Describe ringworm

A

Ringworm is annular (circle) with an elevated edge. This is known as tine corporis. This is a dermatophyte infection (fungus). Tinea means dermatophyte. This will have scaling and small pustules. It is usually annular. Tinea incognito occurs when steroid cream is used as this feeds the infection. The diagnosis is confirmed with skin scrapping and sent to the microbiologists.

69
Q

Describe scabies and how do you treat them?

A

Scabies will have lesions with burrowing marks. This is incredibly itchy so there will be excoriation marks. The mite which causes this is called sarcoptes scabiei. They like to hide between the interphalangeal spaces. All contacts of the patient will need treatment with a scabicide such as permethrin or malathion and all linen will need to be washed. Some patients may develop post scabetic pruritus or eczema.

70
Q

How should headlice be treated?

A

Pediculosis capitis (headlice) are insects which are visible. They live of hairs near the scalp and feed on the blood of the scalp. They can transmit staph aureus or strep pyogenes infections. They can cause secondary eczema and bite marks will be erythematous, papular and very itchy.

Treatment is with wet combing to remove the lice and hair conditioner. Pediculicides can also be used such as malathion, permethrin or dimeticone.

71
Q

How do glucocorticoids work?

A

These are naturally produced by the adrenals in response to ACTH. Glucocorticoids enhance gene expression in target cells which encode for anti-inflammatory proteins. Monomers of the glucocorticoid receptors can also competitively inhibit transcription of inflammatory proteins and immune complexes. All cells express two nuclear receptors for glucocorticoids, a mineralocorticoid and glucocorticoid receptor. This means steroids have an effect on mineralocorticoid function.

Physiological effects of glucocorticoid hormones include metabolic homeostasis, cognition and mental health, reproduction, development, stress response, cell proliferation and inflammation. Therefore, pharmacological effects include anti-inflammatory response and immune suppression. Examples of glucocorticoids commonly used include dexamethasone, prednisolone and hydrocortisone.

72
Q

When should glucocorticoids be used?

A

Indications include auto-immune conditions (rheumatoid arthritis, SLE, and transplant rejections), allergies (Atopic dermatitis and anaphylaxis) and inflammatory conditions such as IBD, asthma and COPD.

When steroids are given pharmacologically this exceeds normal physiological doses. Therefore less CRH is secreted and thus less ACTH. If the steroids are stopped suddenly then there will be a significant drop in steroid concentration which can cause severe illness. Steroids need to be tapered off if they have been used for a significant period of time.

73
Q

What are the side effects of glucocorticoids?

A

Side effects:
1. Metabolic: Hyperglycaemia, insulin resistance, disturbed fat metabolism, hypertension, muscle atrophy and osteoporosis

  1. Immunosuppression: Increased risk of infection, re-activation of latent infections and lymphopaenia
  2. Tissue-specific: Peptic ulcer and GI bleeding, poor wound healing, rash, psychosis and mood changes, sodium and potassium retention, cataracts and glaucoma.
  3. Others such as suppression of rhythmic secretion of steroids and glucocorticoid resistance
74
Q

What is the most common cause of biliary obstruction?

A

The most common cause of biliary obstruction is gallstones and the most common malignant cause is pancreatic cancer (head of the pancreas). Gallstones are most common in the common bile duct.

75
Q

Describe the stages of COPD

A

Stage 1 (Mild): FEV1 80% of predicted value or higher. With these values, a diagnosis of COPD can only be made on the basis of respiratory symptoms

Stage 2 (Moderate): FEV1 50-79% of predicted value

Stage 3 (Severe): FEV1 30-49% of predicted value

Stage 4 (Very Severe): FEV1 less than 30% of predicted value

Medicine Year 3 (22 decks)

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