Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals > Endocrinology & Breast > Flashcards

Endocrinology & Breast Flashcards

1
Q

Definition & Pathophysiology - T1DM

A

Autoimmune destruction of pancreatic beta cells leading to loss of insulin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

S&S - T1DM

A

4Ts - toilet (polydipsia), thin (W/L), thristy (polydipsia) & tired

nausea
vomiting
FTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diagnosis of T1DM

A

Clinical symptoms & random blood glucose >11 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

DKA - pathophysiology

A

Complete lack of insulin leads to a state of hyperglycaemia, glucose cannot be transported into cells as no insulin signal. Blood is hyperglycaemia but body/cells perceived as in a starvation state & so begin ketogenesis.

Over time the patient gets higher and higher glucose and ketones levels. Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH.
Over time the ketone acids use up the bicarbonate and the blood starts to become acidic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

S&S - DKA

A 
Polyuria & Polydipsia
N&V
Abdominal pain 
Leg cramps
Headache
Confusion
Drowsiness 
Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diagnosis of DKA

A

Hyperglycaemia - glucose >11mmol/L
Ketones - +++ on dipstick or cap >3mmol/L
Venous/arterial blood gas: pH < 7.3 or bicarbonate < 15 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of DKA

A 
FIG PICK
Fluids resuscitation
Insulin
Glucose - monitor & add dextrose
Potassium - monitor & correct
Infection - treat underlying causes
Chart - fluid balance
Ketones - monitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of DKA

A

Non-compliance 25%
Inadequate/missed dose of insulin 13%
Infection (30-40%)
Undiagnosed T1DM 10-20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Definition of Hyperthyroidism - types

A

Overproduction of thyroid hormone causing thyrotoxicosis

Primary - issue with thyroid, high T4/T3, low TSH
Secondary - issue with hypothalamic/pituitary, high T4/T3 & high TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aetiology of Hyperthyroidism

A 
Grave's Disease - autoimmune disease, TSHR-Abs 
Toxic multinodular goitre
Solitary toxic adenoma
2 hyperthyroidism - pituitary adenoma
Drugs - amiodarone, T4 overdose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical Features - Hyperthyroidism

A 
Goitre
Palpitations
Heat intolerance
Weight loss
Diarrhoea
Amenorrhoea
Reduced libido
Gynaecomastia (in men)
Fatigue
Change in mood

Signs: Goitre, Sinus tachycardia/arrhythmias, Hair loss, Palmar erythema
Tremor, Thyroid bruit (Graves’), Myxoedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Investigations - Hyperthyroidism

A

Bedside - observations, ECG (sinus tachycardia)
Bloods e.g. FBC (hb - anaemia for tiredness)
Thyroid function tests - fT3/fT4 & TSH
Autoantibodies - TSH-R

Imaging - USS, thyroid uptake scan

NICE also advises screening for T1DM, other AI conditions & new onset AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management - Hyperthyroidism

A

Thioamides (carbimazole or propylthiouracil)
Beta blockers - symptoms
Radioactive iodine
Thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications - Hyperthyroidism

A

A thyrotoxic crisis is rare but potentially fatal result of untreated/undertreated hyperthyroidism.

Beta-blockers
Thionamides: typically propylthiouracil, which in addition to its anti-thyroid effect also reduces the conversion of T4 to T3.
Corticosteroids: reduce the conversion of T4 to T3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Definition & Types - Hypothyroidism

A

Definition: Underproduction of thyroid hormone

Primary - issue with thyroid, low T3/T4 but high TSH
Secondary - issue with pituitary, low T3/T4 & low TSH
Tertiary - issue with hypothalmus, low T3/T4 & low TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes - hypothyroidism

A

AI - Hashimoto’s thyroiditis
Iodine deficiency
Drugs - amiodarone, radioI
Congenital Hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Investigations - Hypothyroidism

A 
Bloods
	• FBC - Hb (r/o anemia)
	• B12 & Folate
	• Autoantibodies - anti-TPO & anti-Tg
Thyroid Function Tests
	• Primary - low T3/T4 & high TSH
	• Secondary - low T3/T4 & low TSH

Imaging
• USS + 2ww if suspicion of malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Clinical features - hypothyroidism

A 
• Weight gain
	• Tiredness/fatigue
	• Cold intolerance	• Goitre
	• Hair loss
		○  characteristically the outer third of the eyebrows
	• Bradycardia
• Dry skin
• Hair loss
• Reduced libido
    o Menstrual irregularities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management of Hypothyroidism

A

Replacement of thyroxine

• Levothyroxine & titrate for control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Complications - Hypothyroidism

A

Often results from acute decompensation during an intercurrent illness. Patients are hypotensive, hypothermic, bradycardic and demonstrate cognitive decline.

IV levothyroxine is the mainstay of management. Electrolyte imbalances and hypothermia should be addressed. IV hydrocortisone may be needed unless hypopituitarism is ruled out as a cause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Definition - Cushing’s Syndrome & Disease

A

Syndrome associated with chronic inappropriate elevation of free circulating cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Aetiology - Cushing’s

A

ACTH-Dependent (80%)
• Excess ACTH secreted from pituitary adenoma –> Cushing’s Disease
• ACTH secreted from ectopic source e.g. small cell lung carcinoma

ACTH-Independent (20%)
• Excess cortisol secreted from benign adrenal adenoma
• Excess cortisol secreted from adrenal carcinoma

Exogenous Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical Features - Cushing’s

A

'’SWEDISH’’ - spinal tenderness/osteoporosis, weight gain, easy bruising, T2DM, intracapsular fat pad, striae, hypertension

Moon Face
Hyperpigmentation
Central obesity
Hiritisum 
Acne 
Frontal Balding
Oligo/amenorrhea
Poor wound healing
Recurrent infections
24
Q

Investigations - Cushing’s

A

Bloods
• Early morning cortisol
• Low dose dexamethasone (1mg) suppression test
○ if cortisol still high then +ve = Cushing’s
Urine
24 hour urinary cortisol; levels 3-4x normal

Localising

  • plasma ACTH (high = acth dependent)
  • high dose dexamethasone (suppressed - pituitary, unsuppressed - ectopic)
25
Q

Management - Cushing’s

A

Surgery - transsphenoidal resection of pituitary adenoma

26
Q

T2DM - Risk Factors

A 
Obesity
Family hx 
PCOS
HX of GDM
Diet
Low birth weight
27
Q

T2DM - Clinical Features

A 
Tiredness/lethargy
Polyuria
Polydipsia
Weight gain
Recurrent infections
28
Q

T2DM - Diagnosis

A

Clinical symptoms + HbA1c >48 or fasting glucose >7

29
Q

T2DM - Management

A

Lifestyle modifications
Metformin (1st line) - if HbA1c stays >58 then + 2nd line
2nd line: sulphonylurea, GLP1 agonists, DDP4i, SLGT2i
Insulin

30
Q

Classes & Examples of Diabetic Drugs

A 
Metformin
Sulphonylurea - gliclazide
GLP1 agonists - liraglutide
DPP4i - sitagliptin
SLGT2i - empaglifozin
31
Q

Breast Cancer - risk factors

A 
• Genetics - BRCA
	• Family history
	• Early menarche & late menopause
	• Age 
	• Nulliparity 
	• Increased age of first pregnancy
	• Combined oral contraceptive (still debated, effect likely minimal if present)
	• Hormone replacement therapy
	• White ethnicity
Exposure to radiation
32
Q

Breast Cancer - Types

A

ductal (in ducts) or lobular (in lobes)

invasive or in situ (not invaded basement membrane)

33
Q

Breast Cancer - Clinical Features

A

• Breast lump - often hard, irregular, immobile
• Axillary lump
• Changes to skin - change to normal experience, skin tethering, peau d’orange, oedema
Nipple changes - new inversion, discharge (bloody = scarier), dilated veins

34
Q

Breast Cancer - 2WW Criteria

A

• Aged 30 or over with breast lump (with or without pain)
• Aged 50 or over with any of the following in one nipple
○ New inversion
○ Discharge
○ Other changes of concern
• Anyone with skin changes worrying for breast cancer
• Aged 30 or over with axillary lump

35
Q

Breast Cancer - Investigations

A

TRIPLE ASSESSMENT
• History & Examination by specialist
• Imaging - mammogram or USS
○ <40s tend to have USS as breast tissue is too dense
○ USS also used if patient has had recent mammogram
• Histopathology
FNA or Core biospy

36
Q

Breast Cancer - Management Options

A

• Surgical
○ Local resection +/- lymph nodes
○ Mastectomy +/- lymph nodes

• Radiotherapy - often used adjunctively (after surgery)
	○ Local 
	○ Whole breast 
	○ Lymph nodes

• Chemotherapy & Biologics
	○ Before surgery 
	○ Chemotherapy regimes 
	○ Herceptin (Trastuzumab) in those with HER2 positive breast cancer

• Endocrine therapy - usual course is for 5yrs
	○ Tamoxifen or Aromatase inhibitors
37
Q

Aetiology - Mastitis

A

Infective - bacteria enters breast via nipple, commonly staph aureus

Non-infective - obstruction of milk ducts & accumulation of breast milk

38
Q

Mastitis - Risk Factors

A 
• Poor attachment to breast
		○ Cleft palate 
		○ Short frenulum 
	• Reduced feeding (in no. or duration)
		○ Rapid weening 
		○ Unilateral feeding 
		○ Breast tenderness 
 • Pressure on breast
	○ Seat belt
	○ Tight Bra 
Sleeping position
39
Q

Clinical features - Mastitis

A

Red hot swollen painful breast - usually unilateral
lymphadenopathy
Signs of systemic upset - malaise, myalgia, pyrexia, tachycardia

40
Q

Management - Mastitis

A

Conservative
• Patient education regarding risk factors
• Encourage to continue breast feeding/expressing
• Analgesia - paracetamol, ibruprofen
Warm compresses & warm bathing

• Some may require antibiotic treatment
• If no improvement with conservative management or if infection is suspected e.g. fever  Flucloxacillin QDS 10-14days
41
Q

Benign Breast Disease

A

Fibroadenoma: Result from hyperplasia of a breast lobule and contain both normal epithelial and connective tissue elements.

Fat necrosis: Irregular and necrotic adipocytes, amorphous material and inflammatory cells, including foreign body giant cells, can mimic malignancy.

Sclerosing adenosis: Is an aberration of normal involution.

Duct ectasia: Occurs when central ducts become dilated with duct secretions; if leakage occurs into periductal tissue, this causes an inflammatory reaction (periductal mastitis).

42
Q

Adrenal Insufficiency - Definition

A

Deficiency of adrenal hormones - glucocorticoids, mineralocorticoids & androgens

43
Q

Adrenal Insufficiency - Types & Aetiology

A

o Primary AI; issues with adrenal glands

  • 80% of cases are due to autoimmune causes - Addison’s
  • Other causes: infection (TB), metastasis, hemorrhage or sepsis

o Secondary AI; issue with pituitary gland

- Lack of ACTH released resulting in low cortisol
- Can be due to pituitary tumour,  infection, loss of blood flow (Sheehan's syndrome)

o Tertiary AI; issue with hypothalamus

- Lack of CRH released usually due to suppression of HPA axis
- Usually due to long term use of steroids
44
Q

Clinical Features - Adrenal Insufficiency/Addison’s

A 
• Fatigue/tiredness
	• Abdominal pain
	• Nausea & vomiting 
	• Cramps
Reduced libido
• Hyperpigmentation
• Postural hypotension 
• Hypotension  Loss of body hair (women)
45
Q

Diagnosis & Investigations - Adrenal Insufficiency/Addison’s

A

U&Es - can show hypoNa & hyperK
Serum cortisol - measured 8-9am

Short synacthen test; synacthen given - cortisol measured, should double in normal patients

Imaging - CT/MRI Adrenals
Can be used if structural pathology suspected

46
Q

Management of Adrenal Insufficiency/Addisons

A

Replacement of steroids - titrated based on S&S & electrolytes
• Hydrocortisone - replaces cortisol
• Fludrocortisone - used in aldosterone in need of replacment
Patient education
• Recognition of Addisonian Crisis (managed with IV hydrocortisone & fluid rehydration)
• Steroid Card & ID tag
Sick day rules - double doses in acute illness

47
Q

Complications of Addison’s

A

Addisonian Crisis – severe dehydration, severe n&v, pale, cold, clammy skin, sweating, rapid, shallow breathing, dizziness, coma
Treat with IV steroids (hydrocortisone), fluids & glucose if needed

48
Q

Types of Hyperparathyroidism & causes

A

Primary = increased PTH (independent on Ca level) due to adenoma, leads to hyperCa

Secondary = increased PTH due to hypoCa, usually as a result of chronic renal failure or vit D deficiency

Tertiary = increased PTH leading to hyperCa due to hyperplasia of gland due to long term secondary HPTH

49
Q

Clinical features of hyperCa vs hypoCa

A

HyperCa - renal stones, bone pain, constipation, N&V, confusion, fatigue

HypoCa - pins & needles, spasms, cramps, wheeze, stridor

50
Q

Causes of hyperCa

A 
Primary or Tertiary HPTH
Malignancy 
Ectopic Vit D production - sarcoidosis 
Thyrotoxicosis 
Drugs - OTC Ca or Vit D or thiazide diuretics
51
Q

Investigations for hyperparathyroidism

A

Bloods - U&Es, calcium, ALP (bone profile), albumin, phosphate, VitD

  1. Serum Ca - high = HPTH
  2. Measure PTH - high = HPTH, low = other cause e.g. malignancy,

Primary HPTH = high PTH, high Ca
Secondary = high PTH, normal/low Ca
Tertiary = high PTH, mega high Ca

Can also consider urine Ca (r/o familial hypocalcuric hyperCa)
Imaging - USS or Xray

52
Q

Management of Hyperparathyroidism

A

Primary HPTH - surgery to remove adenoma or conservative treatment (maintain adequate hydration)

Secondary HPTH - treat cause e.g. renal failure or Vit D supplements

53
Q

Management of hyperCa

A

IV fluids x2
Bisphosphonates

'’Rehydrate, rehydrate, bisphosphonates’’

54
Q

Hyperaldosteronism - Types & Causes

A

Primary hyperaldosteronism (Conn’s Syndrome)

  • Due to issue with adrenal glands, acting independently of RAS
  • Causes include: bilateral idiopathic hyperplasia, adrenal adenoma, familial (rare) & adrenal carcinoma (rare)
    - –> High aldosterone, low renin

Secondary hyperaldosteronism

  • Dysfunctional RAS causes overproduction of aldosterone
  • Causes include: renal artery stenosis, renal artery obstruction & heart failure
    - –> High aldosterone, high renin
55
Q

Clinical features of hyperaldosteronism

A

HypoK
Hypertension
Alkalosis

56
Q

Investigations & Diagnosis - Hyperaldosteronism

A

Serum aldosterone & renin ratios
○ Primary = high aldosterone, low renin
○ Secondary = high aldosterone, high renin

Bloods - U&Es to show hypoK
BP - hypertension

Imaging
o CT/MRI adrenals - adenoma
o Renal doppler - renal a. stenosis

57
Q

Management of Hyperaldosternonism

A
  • Aldosterone antagonists - spironolactone & eplerenone

* Surgical options to treat cause e.g. removal of adenoma or renal a. angioplasty repair

Finals (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions