Brainscape's Knowledge GenomeTM

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


See full index

12: Endocrine System > Chapter 120 Adrenal Glands > Flashcards

Chapter 120 Adrenal Glands Flashcards

1
Q

At what level does left and right adrenal gland site

A

R at T13

L at L2

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

What emvryonic tissue is adrenal cortex derived from? And adrenal medulla?

A

Cortex derived from mesoderm

Medulla derived from neural crest ectoderm (migrates into centre of mesenchymal ball)

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

From which vessels does the adrenal gland receive its arterial supply?

A

Arterial supply

  • Aorta
  • Phrenicoabdominal artery
  • Renal artery
  • Cranial abdominal artery

Venous drainage

  • Single adrenal vein (into cava on R, into renal vein on L)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

WHat are the three layers of the adrenal cortex and what is produced in each layer?

A
  • Zona glomerulosa* = Mineralocorticoids
  • Zona fasciculata* = Glucocorticoids
  • Zona reticularis* = Sex steroids (androgens and oestrogens)

GFR = Salt, sugar, sex

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

What is the (organic chemistry wise) difference between aldosterone and cortisol

A

Aldosteone lacks hydroxyl group on C-17

(Zona glomerulosa (i.e. aldosterone zone) doesnt have the enzyme 17α-hydroxylase)

Adrenal corticoids are synthesized from cholesterol. Enzymatic cleavage of a carbon side chain within mitochondria produces the C-21 steroid pregnenolone. Within cells of the zona fasciculata and zona reticularis, pregnenolone is hydroxylated at C-17 to form the glucocorticoid molecule. Zona glomerulosa cells lack 17α-hydroxylase; absence of a hydroxyl group on C-17 is the major difference between aldosterone and cortisol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is cortisol transported around body

And aldosterone

A

Steroid hormones are lipids so reliant onprotein-binding for transport

Cortisol:

  • 75% bound to transcortin (=cortisol-binding globulin)
  • 15% bound to albumin
  • 10% unbound

Aldosterone:

  • 10% bound to transcortin
  • 50% bound to albumin
  • 40% free
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is transcortin produced?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are cortisol and aldosterone metabolised

A

Liver

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

What is half life of cortisol?

And aldosterone?

A

Cortisol half life 60 minutes

Aldosterone half life 20 mins

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

How is transcortin affected by pregnancy

A

Pregnancy increases hepatic synthesis of transcortin

(wonder why…)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the primary function of glucocorticoids?

List 3 other effects of glucocorticoids

A

Regulation of metabolism

(particluarly by stimulation of hepatic gluconeogenesis)

Other effects:

  • Protein catabolism
  • Protein sythesis inhibition
  • Suppression of inflammatory/immune reponse
  • Gastric acid secretion
  • Vasopressin inhibition
  • Lipolysis stimulation
  • Inhibition of glucose uptake and metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the hormonal axis for glucocorticoids

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

What are the major functions of aldosterone?

A

Electrolye balance

BP homeostasis

(–> retention of water, sodium and chloride, excertion of potassium)

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

Describe the cycle controlling aldosterone release.

A
  • Release of aldosterone is influenced primarily by the RAAS and blood potassium concentrations.
  • Renin, which is produced by the juxtaglomerular apparatus of the kidney, is a proteolytic enzyme that splits circulating angiotensinogeN (synthesized in the liver) into angiotensin I.
  • (Within the pulmonary capillary endothelium) angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE).
  • Angiotensin II stimulates peripheral vasoconstriction and secretion of aldosterone by the zona glomerulosa.
  • Aldosterone in turn promotes sodium, chloride, and water reabsorption and potassium excretion, particularly at the renal tubules.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where is renin produced?

Where is angiotensiongen produced?

Where is ACE produced?

Where is aldosterone produced?

A

Renin: from juxtaglomerular apparatus of kindey

Angiotensinogen: from liver

ACE: from pulmonary capillary endothelium

Aldosterone: from zona glomerulosa of adrenal gland

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

Where are cathecholamines produced?

A

Chromaffin cells of adrenal medulla

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

What is the substrate and enzyme that lead to cathecholamine production

A

Substrate: Tyrosine (and a little bit of phenylalanine)

Enzyme: Tyrosine hydroxylase

Product: Cathecholamines (dopa, dopamine, norepinephrine, epinephrine)

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

What system regulates adrenal medulla

A

Sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the ratio of epinephrine: norepinephrine in dogs?

And in cats?

A

Dogs:

60% epinephrine, 40% norepinephrine

Cats:

70% epinephrine, 30% norepinephrine

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

How are cathecholamines metabolised and extreted?

A

Metabolised by liver

Secreted by kidneys

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

WHat is the primary action of cathecholamines?

A

Acute stress response

Regulation of intermediary metabolism (particularly in response to hypoglycaemia)

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

Describe the action of epinephrine and norepi:

A
  • Actions are mediated through alpha- and beta-adrenergic receptors on target tissues.
  • Alpha-1 and alpha-2 receptors control catecholamine release from presynaptic and postsynaptic sympathetic nerve endings.
  • Beta-1 receptors primarily affect the heart, and beta-2 receptors affect intermediary metabolism and smooth muscle contraction.
  • Epinephrine is approximately 10 times more potent on beta-2 receptors (–> relaxation of smooth muscle in bronchioles, detrrusor muscle, GI, iris) than norepinephrine, so it is more important in controlling metabolism.
  • At beta-2 receptors, epinephrine increases blood glucose concentrations, particularly by promoting hepatic glycogenolysis and gluconeogenesis. Epinephrine also stimulates glycogenolysis in skeletal muscle, with subsequent production of lactate that is converted by the liver to glucose.
  • Epinephrine inhibits insulin secretion (via alpha-2 receptors), stimulates pancreatic glucagon secretion to increase blood glucose concentrations, and promotes lipolysis to increase free fatty acid concentrations in the blood.
  • Epinephrine and norepinephrine interact with beta (1) receptors to increase the force of cardiac contraction and, by shortening the duration of diastolic depolarization, increase heart rate.
  • Norepinephrine causes generalized vasoconstriction through stimulation of alpha receptors, resulting in an increase in vascular resistance and systolic blood pressure. In contrast, epinephrine’s affinity for beta-2 receptors causes vasodilation in skeletal muscle arterioles, coronary arteries, and all veins. Although this reduced peripheral resistance should decrease diastolic pressure, minimal change in blood pressure is usually noted because of the concurrent increase in cardiac output secondary to an increased heart rate and contractility produced by epinephrine.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List 3 features that can used to diagnose an adrenal ‘mass’

A
  • >1.5cm maximum width
  • Loss of typical kidney-bean shape
  • Asymmetric shape and size compared with contrlateral gland
24
Q

List 4 other ddx for an adrenal mass (based on asymmetry)

A
  • Cyst
  • Haematoma
  • Normal hypertrophy
  • inflammatory nodule
25
Q

When is surgical intervention for adrenal mass warranted?

A

If any of below:

  • Functinal
  • Malignant
  • >2cm (“likely to be” malignant)
26
Q

Describe the post-op concerns associated with a functional adrenal tumour secreting:

  • Cortisol
  • Aldosterone
  • Progesterone
  • Testosterone/androstenedione
  • 17-OH progesterone
  • Deoxycorticosterone
  • Epinephrine
A
27
Q

What are c/s of cortisol secreting adrenal tumour

And cbc/biochem/urinalysis changes

A

Hyper-A

  • PUPD
  • Polyphagia
  • Panting
  • Abdo enlargement
  • Mild muscle weakness
  • Lethargy
  • Alopecia

CBC/Biochem

  • Stress leukogram
  • Increased ALP
  • Hypercholesterolaemia
  • Isosthenuria/hyposthenuria
  • Proteinuria
28
Q

In a cortisol secreting adrenal tumoir, what size shoudl contralateral gland be

A

Atrophied

<3mm

29
Q

What test is used to dx HyperA

A

LDDS Test

30
Q

In LDDS test, what is defined as “suppression”

A
  • 4 hours post cortisol of <1.5 ug/dL
  • 4 hours post cortisol <50% of baseline
  • 8 hours post cortisol <50% of baseline

N.B. 60% of pituitary dependent will suppress ‘a bit’. If NO supression then pituitary or adrenal dependent hyperA.

N.B. if adrenal mass + hyperA signs but supresses on LDDS then likely pituitary dependent hyperA AND non-cortisol secreting adrenal mass (especially if contralateral gland not atrophied)

31
Q

What test can be used to distinguish pituitary vs adrenal dependent hyperA if LDDS equivocal?

A

Single baseline plasma ACTH

(Will be high with pituitary dependent. If adrenal tumour ACTH should be low (<10 pg/mL))

(or in theory can do HDDS but not mentioned in the book)

N.B. urine cortisol: creat also good for rule out of hyperA

32
Q

What test is the preferred method for support of phaeo

A

urine creatinine:normetanephrine most specific

(can also measure urine an plasma metanephrone levels)

Can only definitively diagnose with histo

33
Q

What are c/s of phaeo

And pe findings

A

Episodic collapse

Weakness

(Pe

  • Tachycardia
  • Excessive oanting
  • Tacypnoea
  • Weaknes
  • Muscle wastage
  • Retinal haemorrhage/detachment
  • (intermittent arrythmia and hypertension)
34
Q

Aside from the usual testm name one that canbe used to distinguish hyperA (pituitary OR adrenal dependent) from cathecholamine secreting

A

Serum inhibin assays

Inhibin is secreted by ovary/testes and adrenal cortex. Dogs with adrenal- or pituitary-dependent hyperadrenocorticism have consistently elevated levels of serum inhibin (0.82 and 0.16 ng/mL, respectively), whereas healthy dogs or dogs with pheochromocytoma have undetectable levels

35
Q

What pre-op management is recommended in cortisol secreting adrenal tumours

How is this monitored?

A
  • Trilostane 2mg/kg bid
  • After 2 weeks do ACTH stim test (4-6 hours after trilostane)
    • Aiming for post-ACTH cortisol level of 2-5 ug/dL (+improved clinical signs)
  • Also check electrolytes for iatrogenic hypoadrenocorticism
36
Q

How does trilostane work?

A

Trilostane is a competitive inhibitor of 3-β-hydroxysteroid dehydrogenase

Inhibits conversion of pregnenolone to 17α-hydroxyprogesterone (cortisol precursor)

37
Q

List 6 periop concenrs in a hyperA patient

A
  • Impaired wound healing
  • Immunosupppression
  • Hypertension
  • Hypercoagulability
  • Post-op hypoadrenocorticism
  • Pancreatitis
38
Q

How woudl hypertension with hyperA be treated?

A

ACE-I

39
Q

List 3 methods to minimise risk of post-op thromboembolism

When do they usually occur

A
  • Regular movement/walk
    • Appropriate analgesia plan to ensure able to walk soon post-op
  • Minimise GA time
  • ?Minimally invasive approach

<72 hours post-op

40
Q

What are c/s of PTE

How is it doagnosed?

And treated:

A

Signs:

  • Coughing, dyspnoea, tachypnoea, lethargy, haemopsysis, syncope, collapse, sudden death
  • ?crackles/harsh lung sounds, louder or split heart sound

Dx:

  • Bloods: V/Q mismatch and increased Aa gradient on ABG (PaO2 and PaCO2 may be normal)
  • Rads :Alveolar pattern/infiltrates
  • Selective angiography = gold standard
  • CT/MRI (possible but also need restraint)

Tx:

  • Heparin
  • Mechanical ventilation
  • Other supportive
  • +- Theophylline (–> bronchodilation + vasodilation)
  • +- Sildenafil (selective pulmonay artery vasodilation) if pulmonary hypertension documented
41
Q

How should a patient be managed post-op after excision of a cortisol producting tumour?

A

I.e need to address:

  • Poor wound healing
  • Immunosuppression
  • Hypercoagulability
  • Hypoadrenocorticism
  • +- hypertension

Tx:

  • Use non-absorbable sutures for abdo closure
  • Glucocorticoid levels/replacement
    • Consider ACTH stim immediately post-op (pre dex) to assess baseline function
    • Dexamethasone 0.1mg/kg 1st day (alternatively hydrocortisone CRI)
      • If ACTH result confirms hypoadrenocorticism
      • Continue tapering dose dex (0.01 mg/kg bid) until able to give oral meds
      • Then pred 0.5 mg/kg bid
      • After 4 weeks repeat ACTH stim (aiming for Post ACTH of >5 ug/L
    • Mineralocorticois replacement (DOCP) if Na < 135 mmol/L and K >6.5 mmol/L (mild hyponatraemia/hyperkalaemia common after adrenalectomy
      • Re-check electrolytes 25d later. If normal re-check 7 d later.
  • Regular walking (to reduce risk PTE)
  • ACE-I if hypertension
42
Q

How should phaeo be managed pre-op

And intra-op?

A

Pre-op

  • Phenoxybenzamine 0.5 mg/kg bid for 2-3 weeks.
  • (Chapter author increases dose to max dose of 2.5 mg/kg bid or stop if adverse reaction i.e. signs of hypotension)
  • If tachycardia cont despite phenoxybenzamine can add beta blocker (0.2 - 1.0 mg/kg propanolol tid or 0.2-1.0 mg/kg atenolol bid)

Intra-op

  • Avoid drugs that are arrythmogenic, anticholinergic, potentialte effects of cathecholamines or affect alpha receptors
  • Apply moniotring before induction
  • Phentolamine (0.1 mg/kg then 1-2 ug/kg/min CRI) if arterial hypertension
    • Nitroprusside (0.1-0.8 ug/kg/min) if phentolamine not enough
  • Lidocaine (2 mg/kg iv) if pathologic ventricular arrythmia
    • HR >180 bpm
    • Polymorphic complexes
    • R on T
  • Esmolol if tachycardia
43
Q

List 2 benefits of flank approach for adrenalectomy

Where is approach performed

A
  • Less likelihood of wound complications/herniation (poor healing)
  • Better access to ipsilateral adrenal gland

But cant access contralateral and v difficult if vascular invasion

Approach just caudal to last rib and beneath epaxial muscles (then grid approach)

44
Q

How can midline coeliotomy exposure be improved/

A

Extend with paracostal inscision

45
Q

Where are lap ports placed for adrenalectomy

Name an alternative position

A
  • one portal used to place a retractor dorsal to the kidney
  • three remaining portals arranged in a semicircular manner in the paracostal area ventral and caudal to the kidney

Modified approach:

Patient positioned in sternal recumbency, suspended from cushions under the thoracic limbs and the pelvis in order to allow the abdominal viscera to fall ventrally and away from the area of the retroperitoneal adrenal glands

46
Q

Briefly decribe adrenalectomy procedure

A
  • retraction by a surgical assistant
  • removal of the adrenal gland is typically initiated by incising the peritoneum at the lateral aspect of the gland in a region that is distant from the aorta, vena cava, and renal vasculature
  • The phrenicoabdominal vein is isolated, ligated or attenuated with a vessel sealing device, and divided at the lateral aspect of the gland.
  • After the lateral aspect of the gland is free, a small stay suture or atraumatic instrument may be used to grasp the adrenal capsule. The gland is retracted medially, exposing multiple penetrating vessels on its dorsal aspect. Because of the depth of the surgical field, hemostasis of these vessels is facilitated by use of a combination of hemostatic clips and bipolar electrocoagulation or a vessel sealing device.
  • After the adrenal gland is freed from its lateral and dorsal attachments, a plane is developed between the renal vessels and the caudal aspect of the gland. Small adrenal branches that arise from the renal artery must be addressed during this dissection.
    • Malignant tumors may invade renal vasculature or parenchyma. In these instances, concurrent unilateral nephrectomy may be required to achieve complete resection of the tumor.
  • As a final step in resection, the phrenicoabdominal vein is ligated at its entry into the vena cava, and medial fascial attachments of the adrenal gland to the vena cava or aorta are bluntly dissected with right-angled forceps. Particular care is indicated to avoid inadvertent laceration of the cava when dissecting the adrenal gland from the thin-walled vessel.
47
Q

What does vacular invasion by an adrenal tumour suggest

A

Malignant neoplasm

most likely phaeo, then carcinoma.

48
Q

What % of phaeos have vascular invasion?

And adrenocortical?

A

35-55% of phaeos

11-16% adrenocortical

49
Q

How does management of adrenal mass with caval invasion differ from routine adrenalectomy

A
  • Ventral midline approach
  • Consider cooling to 32ºC
  • Place rummel tourniques around cava and renal veins as necessary (see knight paper)
  • Dissect out adrenal tumour aside from thrombus
  • Tighten tourniquets
  • Inscise longitudinally at tumour thrombus entry into cava and perform thrombectomy
  • Release tourniquet (to ensure no air left in cava at venotomy site)
  • Apply partial occlusion vascular clamp over venotomy site
  • Suture with fine 5/0 monofilament suture

Alternatively caval resection may be possible if collateral circulation has developed. Can intentionally stage surgeries and pace ameriod constrictor around cava.

50
Q

What two factors are associated with higher mortality in adrenal masses

A
  • V large tumours
  • Acute adrenal haemoarrhage
51
Q

What is MSt for non-surgically managed dogs with adrenal tumours (+- trilostane depneding on whether cortisol secreting or not)

A

15 - 17 months

52
Q

What is most common funtional tumour in cats

A

Aldosterone secreting = Conn’s syndrome

(91% of feline adrenal tumours are cortical tumours)

53
Q

What are clinical signs of hyperaldosteronism?

And blood results?

How is dx confirmed

A

C/s (basically –> hypertension and hypokalaemia):

  • Weakness
  • Plantigrade stance
  • Neck ventroflexion
  • Blindness (if retinal detachment)
  • Reduced reflexes

Bloods:

  • Hypernatraemia
  • Hypokalaemia

Confirm: check blood aldosterone level

54
Q

What is mortality rate of adrenalectomy in cats

A

23%

55
Q

What is teh proposed pathophys of adrenal tumours in ferrets

What are c/s

How do ferret adrenal tumours differ from cats/dogs

A

Increased GnRH

Alopecia, vulval swellig, behavious changes

Most ferrets have bilat tumours

56
Q

How is bilateral adrenal gland neoplasia in ferret managed

What is mortality rate

A

Subtotal adrenalectomy (i.e. only resect part of R gland)

2% mortality!

15% recurrence

57
Q

How did mortality rate change (following adrenalectomy for phaeo), after changing protocol to include pre-treatment with phenoxybenzamine

A

48% –> 13%

12: Endocrine System (2 decks)

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