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YEAR 3 TCD > WEEK 12 - Abdominal Distention And Weight Gain > Flashcards

WEEK 12 - Abdominal Distention And Weight Gain Flashcards

1
Q

What is the most important structure situated immediately anterior to the Pituitary gland, that produces very characteristic symptoms and signs in patients with a large pituitary tumour?

A

Optic chiasm — compression of this, and associated ‘bilateral hemianopia’, can happen because of an enlarging pituitary lesion

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2
Q

Superior suprarenal artery arising from the _____________ artery – often termed superior adrenal arteries
Middle suprarenal artery arising directly from the _______________ - often termed middle adrenal arteries
Inferior suprarenal artery arising from the ______ artery – often termed inferior adrenal artery

A
  • inferior phrenic
  • abdominal aorta
  • renal
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3
Q

Venous blood is drained via the suprarenal veins with the right suprarenal vein draining into the __________ and the left suprarenal vein draining into the ____________
The adrenal glands have a very rich blood supply, and this accounts for the frequent metastasis of malignancies, such as lung cancer, to the adrenal gland.

A
  • IVC
  • left renal vein
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4
Q

What does the glomerulus structure consist of from blood side to the urine side?

A

Endothelial cells, glomerular basement membrane (GBM), epithelial cells (podocytes)

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5
Q

How is adult poly cystic kidney disease (ADPKD) inherited?

A

Autosomal dominant tract

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6
Q
A
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7
Q

What is metabolic syndrome a triad of?

A

Diabetes, HTN, obesity

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8
Q

What are the different weight classes in terms of BMI?

A
  • healthy weight: 18.5–24.9 kg/m2
  • overweight: 25–29.9 kg/m2
  • obesity I: 30–34.9 kg/m2
  • obesity II: 35–39.9 kg/m2
  • obesity III: 40 kg/m2 or more.
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9
Q

What is orlistat?

A

Pancreatic lipase inhibitor — causes reduced fat absorption

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10
Q

What is Saxenda? Who is it available to?

A

GLP1 analogue — slows gastric emptying, increased satiety

Liraglutide (Saxenda) is available on the NHS as a possible treatment for managing weight in adults, if they have: a body mass index (BMI) of at least 35 (or at least 32.5 for some black or ethnic minority people, because their weight-related health risks can be higher at a lower BMI); high blood sugar, which increases their risk of developing diabetes, and high risk of cardiovascular problems such as heart attacks and strokes.

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11
Q

Surgical management of obesity is available for who?

A
  • If BMI > 40 or BMI 35-40 with other significant weight-related disease
  • Tried all non-surgical approaches
  • Has been or is willing to receive Tier 3 weight management services
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12
Q

What are indications for referral to Tier 3 care?

A
  • the underlying causes of being overweight or obese need to be assessed
  • the person has complex disease states or needs that cannot be managed adequately in tier 2 (for example, the additional support needs of people with learning disabilities)
  • conventional treatment has been unsuccessful
  • drug treatment is being considered for a person with a BMI of more than 50 kg/m2
  • specialist interventions (such as a very-low-calorie diet) may be needed
  • surgery is being considered.
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13
Q

What are indications for consideration for bariatric surgery?

A

Bariatric surgery is a treatment option for people with obesity if all the following criteria are fulfilled:

  • They have a BMI of 40 kg/m2 or more, or between 35 kg/m2 and 40 kg/m2 and other significant disease (for example, type 2 diabetes or high blood pressure) that could be improved if they lost weight.
  • All appropriate non-surgical measures have been tried but the person has not achieved or maintained adequate, clinically beneficial weight loss.
  • The person has been receiving or will receive intensive management in a tier 3 service
  • The person is generally fit for anaesthesia and surgery.
  • The person commits to the need for long-term follow-up.

The option of choice (instead of lifestyle interventions or drug treatment) for adults with a BMI of more than 50 kg/m2 when other interventions have not been effective.

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14
Q

What are symptoms of cushing’s disease?

A
  • moon face
  • buffalo lump
  • easy bruising
  • pendulous abdomen
  • amenorrhea
  • stretch marks (violaceous striae)
  • adrenal hyperplasia
  • excess hair growth (hirsutism)
  • thinning of hair and hair loss
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15
Q

What are features that best discriminate Cushing’s syndrome? (Most do not have a high sensitivity)

A

Easy bruising

Facial plethora

Proximal myopathy (or proximal muscle weakness)

Striae (especially if reddish purple and > 1 cm wide)

In children, weight gain with decreasing growth velocity

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16
Q

What are some Cushing’s syndrome features in the general population that are common and/or less discriminatory?

A
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17
Q

What are some Cushing’s syndrome features in children?

A

Slow growth

Abnormal genital virilization

Short stature

Pseudoprecocious puberty or delayed

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18
Q

What signs do you note that are relevant to Cushing’s?

A
  1. Truncal obesity
  2. Gynaecomastia
  3. Striae
  4. Normal body hair distribution
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19
Q

Describe the dexamethasone suppression test

A
  • Dexamethasone is an exogeneous steroid that will cause suppression of the pituitary through negative feedback
  • It is used to assess the integrity of the hypothalamo-pituitary-adrenal axis.
  • Dexamethasone binds to glucocorticoid receptors in the pituitary and thereby inhibits ACTH secretion by the pituitary gland.
  • When testing the adrenal functions in patients with Cushing’s syndrome, Dexamethasone may be administered in low (1–2 mg) and/or high (8 mg) doses.
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20
Q

What happens in the dexamethasone suppression test in a normal person?

A

Reduction in cortisol levels following low-dose dexamethasone

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21
Q

What happens in the dexamethasone suppression test in a person with Cushing’s disease?

A

No reduction in cortisol output after low-dose dexamethasone, but inhibitor of cortisol output following high-dose dexamethasone

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22
Q

What happens in the dexamethasone suppression test in a person with an adrenal tumour or ectopic ACTH?

A

No reduction in steroid production after low or high dose dexamethasone

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23
Q

In patients with high resting cortisol and ACTH levels, and failure of suppression of ACTH with low or high dose Dexamethasone, what should be considered?

A

Ectopic ACTH secretion

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24
Q

What is cyclical Cushing’s?

A

a very rare entity characterised by alternating excess and normal endogenous cortisol secretion and thus can have variable clinical features. If clinical suspicion is high, even if the initial tests are negative, a repeat follow up testing is required. Urinary free cortisol or late-night salivary cortisol are preferred screening options.

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25
Q

What are the ACTH dependent causes of Cushing’s syndrome? (About 80%)

A
  • pituitary adenoma = Cushing’s DISEASE
  • ectopic ACTH 5-10% (bronchial carcinoid commonest)
  • unknown source of ACTH <1%
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26
Q

What are the ACTH independent causes of Cushing’s syndrome? (About 20%)

A
  • adrenal adenoma : 10-18%
  • adrenal carcinoma : 6-8%
  • adrenal hyperplasia
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27
Q

What is the next step after a hypercortisolemic statue is confirmed using initial tests?

A

Measure ACTH: arrange ACTH levels to determine ACTH dependent CS or ACTH independent CS to differentiate the underlying cause

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28
Q

What does it mean if ACTH <5 pg/mL?

A

= ACTH-independent CS

—> arrange CT adrenals to assess adrenal tumour or hyperplasia

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29
Q

What does it mean if ACTH >20 pg/mL?

A

= ACTH dependent CS

—> Arrange a pituitary MRI; presence of pituitary adenoma > 6mm, is highly consistent with Cushing’s Disease.
—> Arrange non-invasive tests (High-Dose Dexamethasone Suppression Test (HDDST) and Corticotropin-Releasing Hormone (CRH) stimulation test, if consistent confirms Cushing’s Disease.

30
Q

What does it mean if ACTH 5-20 ng/mL?

A

= INTERMEDIATE ACTH

—> Repeat testing and if value remains consistently intermediate then consider Corticotropin-Releasing Hormone test (CRH). The presence of ACTH response suggests ACTH Dependent (Cushing’s Disease), while absence of a response suggest ACTH Independent (Adrenal disease) or ectopic ACTH secretion.
—> Arrange Inferior Petrosal Sinus Sampling (IPSS) with CRH stimulation for individuals with unclear MRI (lesion <6 mm) or non-concordant HDDST+CRT to distinguish between ectopic ACTH secretion and Cushing’s Disease.

31
Q

What needs to be replaced after removing all or part of the anterior pituitary gland?

A

The hormones affected and needing replacement could be any of those produced from the anterior pituitary gland:
- TSH (Thyroxine)
- GH (growth hormone therapy in selected few)
- ACTH (hydrocortisone therapy)
- FSH/LH (Testosterone or Oestrogen/Progesterone hormone replacement).

Prolactin does not need to be replaced. The posterior pituitary hormones:
(ADH, Endorphins, Oxytocin) do not need replacement as they are not secreted by the pituitary gland but merely stored.

Only, few cases require Desmopressin (synthetic ADH) where ADH secretion is affected because of the damage to posterior pituitary or hypothalamus causing Diabetes Insipidus

32
Q

What pituitary tumours can occur?

A

Pituitary tumours are benign adenomas of the anterior pituitary. The adenomas are broadly classified by size and the cell of origin.

Pituitary microadenomas are less than 1cm in size and macroadenomas are more than >1 cm.

Adenomas arising from different cells are as below:

Gonadotroph adenoma – mostly non-functioning
Thyrotroph adenoma – TSH producing
Corticotroph adenoma – ACTH producing (Cushing’s disease)
Lactotroph adenoma – Prolactin producing
Somatotroph adenoma – GH producing (Acromegaly)

About 65-70% are functioning adenomas producing one or more hormones and the rest (25-30%) are clinically non-functioning.

33
Q

Describe the short ACTH stimulation test (aka teh tetracosactrin or short Synacthen test)

A

assesses adrenocortical functional activity in response to the injection of exogenous ACTH (tetracosactrin). Cortisol levels fail to increase in response to exogenous ACTH in patients with chronic adrenal insufficiency

34
Q

Short synacthen test low vs high ACTH level result meaning

A

High ACTH levels are associated with adrenocortical failure due to adrenal disease (primary adrenal failure or Addison’s disease)

Low ACTH associated with adrenocortical failure due to pituitary or hypothalamus disease and or lack of ACTH/corticotropjin releasing hormone (secondary/tertiary adrenal failure)

35
Q

_______________ is due to elevated levels of ACTH and hence only seen in Addison’s Disease

A

Hyperpigmentation

36
Q

The electrolyte disturbance and significant postural hypotension are due to lack of ________________ (due to hypovolaemia and sodium loss) and hence commonly noticed in Addison’s Disease

A

Mineralocorticoids

37
Q

What are symptoms of Addison’s disease?

A
  • bronze pigmentation of skin
  • changes in distribution of body hair
  • GI disturbances
  • weakness
  • weight loss
  • postural hypotension
  • hypoglycaemia
38
Q

How should Addison’s Disease be managed?

A

Life-long cortisol replacement with Hydrocortisone, which remains the main stay.

The patient would need to undergo steroid education, understanding of sick day rules and to double the dose of steroid in various circumstances.

They should be taught how to use parental hydrocortisone in event of emergency, or if unable to take steroid orally. They would need mineralocorticoid replacement using Fludrocortisone.

39
Q

What is Adrenal Insufficiency? And how is it different from Addison’s crisis?

A

Adrenal insufficiency is primarily inadequate secretion of cortisol and/or aldosterone to maintain normal physiological function. It can have variable presentation, hence needs a high index of suspicion because if missed it can be potentially fatal.

40
Q

Primary vs secondary vs tertiary adrenal insufficiency

A

Primary — Adrenocortical failure due to adrenal disease

Secondary — Adrenocortical failure due to pituitary disease and or lack of ACTH

Tertiary — Adrenocortical failure due to hypothalamus disorder/lack of corticotrophic releasing hormone

41
Q

What is the most common cause of secondary adrenal insufficiency?

A

The most common cause is secondary adrenal insufficiency due to abrupt withdrawal of chronic glucocorticoid therapy or pituitary disease

42
Q

Primary adrenal insufficiency or Addison’s Disease is most commonly due to what?

A

Auto-immune process in Western population

43
Q

Other than auto-immunity what are other reasons for Addison’s disease?

A
  • Infections (Tuberculosis, HIV/AIDS)
  • Infiltration (Malignancy, Amyloid, Lymphoma, haemochromatosis)
  • Haemorrhage/Infarction
  • Surgical removal (bilateral adrenalectomy)
  • Medications (metyrapone, ketoconazole)
  • Adrenal leukodystrophy (rare)
44
Q

Chronic adrenal insufficiency presents insidiously with various non-specific symptoms, but _____, _______ and __________ are the commonest. The diagnosis is confirmed with the_________________ Test and subsequent investigations to explore the underlying cause. Long-term treatment is always with ___________ replacement therapy and usually, but not always, ______________ therapy (most needed in primary adrenal insufficiency).

A
  • fatigue
  • weakness
  • weight-loss
  • short ACTH (Synacthen) stimulation test
  • glucocorticoid
  • mineralocorticoid
45
Q

Addisonian crisis or acute adrenal crisis: patients with adrenal insufficiency can present with acute crisis leading to circulatory shock and severe hypotension, hyponatraemia, hyperkalaemia, metabolic acidosis, and possible hypoglycaemia. The precipitant factors are intercurrent _____, ______, or _______.

A

Disease, surgery or infection

46
Q

Addisonian crisis or acute adrenal crisis management

A
  1. Correct the volume depletion
  2. Replace glucocorticoids parentally
  3. Correct metabolic abnormalities
  4. Identify the underlying cause
  5. Patient education before discharge, to prevent further occurrence
47
Q

Zona glomerulosa

—> hormone produced, pathology related to this area of the adrenal gland

A

Mineralocorticoids eg. Aldosterone

—> conn’s syndrome

—> adenoma of ZG. Excess aldosterone results in electrolyte imbalances and hypertension

48
Q

Zona Fasiculata

—> hormone produced, pathology related to this area of the adrenal gland

A

Glucocorticoids eg. Cortisol and corticosterone

—> Cushing’s syndrome. Adrenal tumour resulting in excess glucocorticoid secretion

49
Q

Zona Reticularis

—> hormone produced, pathology related to this area of the adrenal gland

A

Androgen precursors eg. DHES and androstenedione (converted to testosterone or oestrogen by gonads)

—> congenital adrenal hyperplasia. Results in lack of mineralocorticoids and glucocorticoids and excess of testosterone and its derivatives

50
Q

Medulla

—> hormone produced, pathology related to this area of the adrenal gland

A

Catecholamines eg. Adrenaline and noradrenaline

—> phaeochromocytoma. Neuroendocrine tumour of adrenal medulla. Excess secretion of adrenaline resulting in tachycardia, HTN, anxiety, palpitations and weight loss

51
Q

What is metyrapone?

A

A glucocorticoid synthesis inhibitor.

It words by inhibiting 11-beta-hydroxylase, thereby inhibiting synthesis of cortisol from Deoxycortisol and the synthesis of Deoxycorticosterone in the adrenal gland

52
Q

ACE inhibitors can lead to an increase in a substance called ___________. This can irritate the airways, triggering inflammation and coughing.

A

Bradykinin

53
Q

What is diabetes insipidus?

A

A rare condition

  • where either too little vasopressin is produced by the pituitary — cranial diabetes insipidus — or the kidney becomes insensitive to vasopressin and does not make aquaporin channels and re absorb water from the collecting ducts — nephrogenic diabetes insipidus
  • in these conditions large quantities of dilute urine are produced — polyuria — and to compensate people drunk large quantities of water — polydipsia
  • If people are unable to drink water they will develop high body sodium levels, hypernatraemia, and become dehydrated. This is the basis of the water restriction test to diagnose diabetes insipidus.
54
Q

What is SIADH and what causes it?

A

Much more common than diabetes insipidus

Many stimuli can override osmolality control and cause the release of inappropriately high amounts of ADH which causes reabsorption of water from collecting ducts and causes urine to have high sodium content or osmolality while serum sodium levels drop (hyponatraemia) as water is retained.

Diagnosis is made by checking paired serum osmolality and urine osmolality and finding serum osmolality is low whilst urine osmolality is high.

Causes of SIADH:

Lung diseases – cancer, pneumonia
Brain lesions – tumour, head injury and bleed, stroke
Drugs – e.g., carbamazepine, selective serotonin reuptake inhibitors (SSRIs), miscellaneous causes

55
Q

What is the clinical approach to hyponatraemia?

A
56
Q
A
57
Q

What can cause:

+++ blood, no protein,

no nitrates, no leucocytes

A
  • menstrual cycle
  • anti-platelet therapy
  • malignancy of kidney, ureter or bladder
58
Q

What can cause:

no blood, +++ protein,

no nitrates, no leucocytes

A

Nephrotic syndrome

59
Q

What can cause:

Bland sediment

A

Normal

60
Q

What can cause:

++ blood, no protein,

++ nitrates, ++ leucocytes

A

UTI, renal stones

61
Q

What can cause:

++ blood, ++ protein,

no nitrates, no leucocytes

A

Nephritic syndrome

—> the name given to a collection of different signs and symptoms that occur as a result of inflammation in the kidneys. This inflammation causes the kidneys to work less effectively. It also causes protein and red blood cells to leak from the bloodstream into the urine. Patients can present as having haematuria, elevated blood pressure, decreased urine output, and oedema.

62
Q

most commonly, what do nephrotic vs nephritic patients present with in their urine?

A

most commonly, nephrotic patients present only with protein in urine, whereas nephritic patients with blood and protein in urine

63
Q

Mild nephritic vs severe nephritic vs nephrotic

A
64
Q

What is the classical triad in renal cancer?

A

Flank pain, haematuria and renal mass with abdominal distension

65
Q

Nephritic and nephrotic syndrome can present with abdominal distension and lower limb oedema due to _________ that results in fluid shift to third space causing oedema and ascites

A

Low albumin

66
Q

What are the 3 most common causes of nephrotic syndrome?

A
  • FSGS = focal segmental glomerulosclerosis
  • minimal change disease
  • membranous nephropathy
67
Q

What is the classical triad of nephrotic syndrome?

A

Proteinuria >3-3.5 grams, hypoalbuminemia, and oedema

Hyperlipidaemia (due to liver compensating for loss of albumin in urine) and loss of other proteins like antithrombin 3 and immunoglobulins are common associations, which makes those patients at high risk for both venous thromboembolism and infections.

68
Q

Is nephritic or nephrotic syndrome more aggressive in presentation?

A

Nephritic syndrome is more aggressive

Patients can present with severe acute kidney injury, oliguria, and hypertension

69
Q

What is the gold standard for diagnosing nephritic and nephrotic syndrome?

A

Renal biopsy

70
Q

Didn’t finish

A

Loser

YEAR 3 TCD (15 decks)

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