1
Q
Forme la plus fréquente de CS
A
PDH 80-85%<br></br>
2
Q
Mean age at diagnosis CS
A
11 years [6m-20y]
3
Q
Sexual status effec CS
A
Neutering predispose
4
Q
Pupd in CS ?
A
Inhibition of VP action (tubular) + increased neurohypophysis threshold release or CDI (large pituitary tumors)
5
Q
Potbelly in CS ?
A
Hepatomegaly, fat accumulation in the abdomen, enlarged bladder + decreased muscle tone
6
Q
Panting in CS ?
A
Decreased pulmonary compliance, respiratory muscle weakness, or PH
7
Q
Pseudomyotonia histo CS
A
Noninflammatory degenerative myopathy
8
Q
Uncommon reproduction abnormalities in CS
A
Prolonged anestrus in females, testicular atrophy in males
9
Q
Acute complication of ectopic thyroid carcinoma
A
Thoracic hemorrhage
10
Q
Adrenal secondary hyperPTH csq of ?
A
Lower urinary P secretion and increased renal Ca excretion
11
Q
Enzyme protective to Mineralocorticoid receptor from cortisol ?
A
11-beta-hydroxysteroid dehydrogenase
12
Q
Why mild hyperNa and hypoK in CS ?
A
High cortisol concentration saturates 11 beta dehydrogenase-> access to MR type 1 -> cortisol-induced mineralocorticoid effect
13
Q
11 beta hydroxysteroid dehydrogenase type 2 and cortisol ?
A
Aldosterone and cortisol same affinity for MR but cortisol higher concentration-> transform cortisol in cortisone (inactivation) -> distal tubule, colon …
14
Q
Frequency eosinopenia in CS
A
54-81 %
15
Q
Frequency thrombocytosis in CS
A
37-78%
16
Q
Frequency lymphopenia in CS
A
14-80%
17
Q
Frequency neutrophilia in CS
A
24%
18
Q
Frequency erythrocytosis in CS
A
10-14 %
19
Q
Frequency monocytosis in CS
A
30%
20
Q
Possible causes of erythrocytosis in CS
A
Bone marrow stimulation, hypoxemia: hypoventilation and obesity (Pickwick syndrome), PT
21
Q
% increased in BG in CS
A
20-57%
22
Q
Duration of bolus insulin secretion in dogs and magnitude of increase
A
6-9 hours, 5-7 fold
23
Q
Duration of bolus insulin secretion in cats and magnitude of increase
A
6- > 12h, 0-3 fold
24
Q
Duration of bolus insulin secretion in human and magnitude of increase
A
2-4h, 5-fold
25
% of dogs with hypercortisolism had concurrent DM
5-22%
26
% of diabetic CN had concurrent hypercortisolism
23%
27
% increased pre prandial bile acids in CS
12%
28
% increased post prandial bile acids
37%
29
USG in general in CS
< 1.020
30
UPC>1 in CS %?
45%
31
UPC> 0.5 in CS %?
70%
32
% bacteriuria/positive culture and LUT signs in CS
10-50% but <5% of LUT signs
33
% hypercoagulability in CS
80%
34
Common abnormalities in coagulation parameters in CS ?
Decreased PT, increased fibrinogen, increased thrombin-antithrombin complexes
35
TT4, fT4, TSH in CS
Decreased TT4/T3 40-60%, decreased fT4 24%, TSH usually normal
36
Mechanisms of disturbed thyroid function in CS
Alteres hormone binding, peripheral metabolism
37
Se and Sp of LDDST
Se= 85-100% ; Sp= 44-73%
38
LDDST consistent with PDH
Suppression of >50% from the basal [cortisol] at 4 or 8 hours (with confirmed HC)
39
LDDST: lack of suppression, PPV
4h, 8h, above the lab cut-off (28-39 nmol/L) and both >50% basal [cortisol]. PPV= 94%
40
LDDST: partial suppression, PPV
Suppression of >50% from the basal [cortisol] at 4h or 8h. Above the lab cut-off but either <50% basal [cortisol]. PDH compatible. PPV= 68%
41
LDDST: escape pattern. PPV
4h below lab cut-off and 8h above lab cut-off. PPV= 37%
42
LDDST: inverse pattern. PPV
At 4h > lab cut-off and at 8h < lab cut-off. Equivocal. Further imaging required. PPV= 37%
43
UCCR: Se and Sp
Se= 75-100% ; Sp= 20-25%
44
ACTHst: Se;Sp PDH vs AT
PDH: Se= 80-83% ; Sp= 59-83%
AT: Se= 57-63% ; Sp= 59-93%
-> dowregulation of ACTH-receptor (MC2R) in adrenocortical carcinoma
45
Pituitary enlargment, P/B value
P/B > 0.31 mm/mm²
46
P/B value increased in HC ?
64% of dogs with dexamethasone-resistant HC
47
48
US: more reliable markers of AT
Smaller gland thickness < 4-5 mm ; heterogenous appearence of the gland
49
Most reliable criteria for malignant AT
Adrenal size > 2 mm and vascular invasion
50
PDH survival without treatment
Median ST= 359-506 days
51
Hypophysectomy in PDH (remission, % of survivors)
94% alive after 4 weeks; remission in 92% of survivors
52
Hypophysectomy in PDH: recurrence
27%
53
Hypophysectomy in PDH: MST, MDFI
MST= 781 days [0-3808]
MDFI= 951 days [31-3808]
54
Hypophysectomy in PDH: % of dogs needed VP lifelong + other supplementation
GC and T4 lifelong; 10% VP lifelong
55
The most common complications of hypophysectomy in PDH
Perioperative death, transient mild hyperNa, CDI, recurrence of HC, transient reduction or cessation of tear production
56
Negative prognostic factor for hypophysectomy in PDH
High P/B value, old age, increased preoperative eACTH and UCCR, dexamethasone resistance on endocrine testing
57
Disadvantages of RT and MST
Numerous anesthesia if not stererotactic, only gradual reduction in tumor size over 1-16 months, not usually eliminate hypersecretion of ACTH (need usually trilostane). MST= 539-1405 days. Stereotactic shorter: MST= 245 days
58
Perioperative mortality adrenalectomy salle AT vs invasive AT
<10% vs 24%
59
Reported HC recurrence after adrenalectomy
12-30% due to AT regrowth, functional métastases or development of PDH
60
Factor associated with survival after adrenalectomy
Associated: AT diameter, thrombus extending beyond the diaphragm, AT > 3 cm
Not associated: venous invasion (vena cava also), capsule rupture, surgery duration, medical TT before surgery
61
Thrombus, survival, adrenalectomy
40% of dogs survival with a thrombus extends beyond the diaphragm vs 73-81% if thrombus terminated before
62
Mechanism of trilostane
Synthetic steroid analogue. Competitive inhibition of 3 beta-hydroxysteroid dehydrogenase. Increase ACTH secretion and increase renine activity. Possibly affects 11-beta-dehydroxysteroid dehydrogenase
63
Rare AE of ACTH administration
Pituitary apoplexy and adrenal hemorrhage
64
Mechanisms of action of mitotane
Adrenocortical necrosis and atrophy.
Inhibition of CYP11A1 (cytochrome P450 cholesterol side-chain cleavage enzyme) + CYP11B1 (11-beta hydroxylase) => contribution to cortisol synthesis Inhibition + activation of CYP3A4= increased metabolic clearance of GC. New: Inhibition of SOAT1 (sterol-O-acetyl-transferase 1) -> increase the amount of free cholesterol in adrenocortical cells -> ER stress -> celle apoptosis
65
Protocole mitotane
Induction phase: 50-75 mg/kg PO (divided in 3-4 portions) with food for 5 days. The q48h for 40 days. Replacement therapy day 3: cortisone acetate 2 mg/kg/day, 0,012 mg/kg/day fludrocortisone acetate, 0,1 g/kg NaCl (q12h for all). After completing initial course: 0,5-1 mg/kg/day cortisone. To prevent recurrence: 50-75 mg/kg PO once weekly for at least 6 months
66
Investigational therapies for new adrenal-target treatments
MC2R antagonists
Steroidogenic factor-1 inverse agonists
Novel SOAT1-inhibitors
67
3 receptor subtypes targeting drugs to treat PDH
DA receptor subtypes 2 (DRD2); SST receptor subtype 2 (SSTR2); SST receptor subtype 5 (SSTR5)
Primary receptor subtype expressed in canine corticotroph adenoma : SSTR2
68
2 molecules with inhibitory fonction on pituitary secretion
Somatostatin and dopamin
69
Carbegoline's target
Dopamin agonist binds to DRD2
70
Difference in target between Pasireotide and Octreotide
Pasireotide: SST analog binds to SST receptors 1,2,3 and 5
Octreotide: SSTR2 with high affinity and SSTR3-5 moderate affinity
71
% of hypertension in dogs with HC untreated
37-86%
With 50% severe hypertension (>180 mmHg)
72
Which dogs with SH and HC at higher risk for target organ damage ?
Thrombocytosis, hypokalemia, and/or proteinuria
73
Mecha for SHT in HC ?
Increased mineralocorticoid activity, decreased NO concentrations, Increased renal vascular resistance
74
Most common comorbidities in HC ?
DM
75
Mechanisms of HC-induced DM
Insulin resistance, increased hepatic gluconeogenesis, beta-cell dysfunction: decrease insulin secretion, blunting incretin effect, direct cytotoxicity
76
% of GBM in dogs with HC
1,6-2,3 %
77
% of dogs with GBM having HC
3-23%
78
Mechanisms of GBM with HC
Higher concentration of unconjugated bile acids due to cortisol excess in EH biliary tree-> more hydrophobic = injury to the biliary epithelium-> mucinous hyperplasia + impaired secretion of DHEA
79
Medical consequences of GBM + HC
- concurrent diagnosis of HC at time of cholecystectomy = 2 fold increase in odds odds death/ control dogs
- higher dosages of trilostane to control HC (lipid-soluble drug, but decrease ability to secrete bile)
80
% of urolithiasis in HC and nature
3% oxCa
81
Causes of hypercoagulability in HC
Increased fibrinogen concentrations, decreased hyperfibrinolysis, and/or thrombocytosis
82
Parameters in Utrecht score
% of cells clear/vacuolated cytoplasm, presence of necrosis, Ki-67 index
To assess post-surgery prognosis
83
% DM in fHAC
80%
84
Dermatological signs in fHAC compared to cHAC
Alopecia less frequently, can be abdominal, cornificatiin defects/seborrhea common (15%)
85
fHAC: cortisol post-stim< 400 nmol/L ; < 40 nmol/L; > 400 nmol/L
HAC not excluded; consider iatrogenic HAC; very likely
86
fHAC: 2 cut-off for DST unlikely and very likely
At 8h: cortisol<40 nmol/L => unlikely ; > 40 nmol/L => very likely
87
Mechanism of metyrapone
Inhibitor of 11-beta-hydroxylase enzyme converts 11-deoxycortisol to cortisol
88
Prevalence of SHT in fHAC vs in cHAC
20% vs 37-86%
89
Why not use 0.01 mg/kg for DST in cats ?
Because 20% of healthy cats not suppress
90
DST in fHAC: 0.01 mg/kg may be useful if
Normal suppression => HAC very unlikely
91
6 tumors more frequently metastasized to adrenals (and not adrenal tumors); % of adrenal masses due to metastasis (dogs vs cats)
Dogs: 27% ; Cats: 60%
Pulmonary, mammary, gastric, prostatic, pancreatic carcinomas and melanoma
92
If primary ATs, % of adrenocortical vs neuroendocrine
75% vs 25%
93
% of adrenal incidentaloma in dogs
4%
94
% of malignancy in incidentaloma in dogs
28,5%
95
% of bilateral PCCs
10% bilateral
90% unilateral
96
% of local invasion into adjacent vessel with PCCs
56%
97
% metastasis in PCCs
20%
98
Why measurement of normetanephrine/metanephrine rather than epi/norepinephrine?
Normeta/meta => production and secretion in tumor cells: continuous and accurately reflects tumor mass
Epi/norepi: episodic secretion
99
Diagnostic accuracy to distinguish adrenocortical to medullary tumors with cytological analysis
87%
100
Bilateral and unilateral mass in hyperaldosteronism
Bilateral: 15% ; unilateral: 85%
101
Hypertension and heart remodeling
Left ventricular hypertrophy
102
What are the **non-tumor possibilities** for an adrenal mass?
* Nodular hyperplasia
* Cyst
* Abscess
* Hematoma
* Granuloma
## Footnote
Not all adrenal masses are primary adrenal tumors.
103
What percentage of canine and feline adrenocortical tumors were found to be **metastatic lesions** in one study?
* 27% in canines
* 60% in felines
## Footnote
This highlights the potential for adrenal masses to be secondary to other cancers.
104
What types of tumors can occur in the adrenal cortex?
* Primary adrenocortical tumors (benign or malignant)
* Myelolipomas
* Lipomas
## Footnote
Primary adrenocortical tumors may or may not be functional.
105
What is the estimated incidence of **IAGM** identified with US in dogs? and by CT?
About 4%; 9%
## Footnote
Most affected dogs are middle-aged or older.
106
What imaging characteristics do not help differentiate between **adrenal adenoma and carcinoma**?
* Mineralization
* US echogenicity
## Footnote
Both adenomas and carcinomas can exhibit these characteristics.
107
What findings on **ultrasound** may suggest malignancy?
* Suspected metastases to abdominal organs
* Evidence of invasion into surrounding tissues
* Tumor size >2 cm
## Footnote
These factors increase the likelihood of malignancy.
108
What are the suggestive features of malignancy on **CT scans**?
* Poor glandular demarcation
* Irregular contrast enhancement
* Non-homogenous texture
## Footnote
These features can indicate a malignant process.
109
What is the role of **contrast-enhanced CT** in evaluating adrenal masses?
High accuracy in confirming vascular invasion
## Footnote
It can differentiate tumor types and assess malignancy.
110
Under what conditions should a **more conservative approach** be adopted for IAGM?
* No evidence of malignancy
* No worrisome clinical signs
* Routine blood/urine tests not indicative of functional AT
* Mass <2 cm in diameter
## Footnote
These criteria help determine when to avoid aggressive treatment.
111
How often should **US monitoring** be conducted for IAGMs?
Monthly
## Footnote
This monitoring can document the mass’s rate of growth and/or change in appearance.
112
What should be done if the IAGM is **enlarging** or changing in appearance?
Adrenalectomy is warranted
## Footnote
This is necessary if the mass compresses or infiltrates surrounding tissues or if clinical signs of excess hormone secretion develop.
113
What was the **median survival** without surgery in 14 dogs with non–cortisol-secreting AT?
29.8 ± 8.9 months
## Footnote
The range of survival was from 1.0 to 96.0 months.
114
What is the relationship between **tumor size** and survival in dogs with non–cortisol-secreting AT?
Larger tumor size is associated with shorter survival
## Footnote
This highlights the impact of tumor characteristics on prognosis.
115
Aldosterone acts on the **distal nephron** to promote which two processes?
* Na reabsorption
* Excretion of K and hydrogen
## Footnote
This action helps conserve sodium and indirectly conserve water.
116
What type of tumors are primarily responsible for **feline primary hyperaldosteronism**?
* Adrenocortical carcinoma
* Adenoma
* Bilateral adrenal adenomas
## Footnote
The tumoral form of PHA is usually due to a solitary tumor.
117
What is the **median age** for diagnosing PHA in cats?
About 13 years
## Footnote
PHA is most commonly diagnosed in cats older than 10 years.
118
Hypokalemia is more common than **hypertension** in cats with what condition?
Adrenal tumors (AT)
## Footnote
The opposite is true for cats with PHA due to hyperplasia.
119
Muscle weakness in cats with hypoK is likely to occur at K concentrations less than _______.
<2.5-3 mmol/L
## Footnote
This level indicates significant potassium deficiency.
120
Common owner concerns for cats with PHA include _______.
* Cervical ventroflexion
* Hindlimb weakness
* Difficulty jumping
* Listlessness
* Ataxia
## Footnote
These symptoms are associated with neuromuscular effects of hypoK.
121
What serious condition can occur with profound **hypoK**?
Respiratory failure
## Footnote
This highlights the critical nature of potassium levels in cats.
122
About **50%** of PHA cats have increases in which laboratory values?
* Urea (blood urea nitrogen)
* Creatinine
* Creatine kinase (CK)
## Footnote
Increases in CK can be quite severe.
123
What is the threshold for PACs that may indicate primary hyperaldosteronism?
>1000 pmol/L (>36 ng/dL)
## Footnote
This concentration can overlap with secondary hyperaldosteronism, especially in cats with CKD.
124
What does **Plasma Renin Activity (PRA)** indicate in the context of diagnosing PHA?
PRA should be within or below the reference range in PHA
## Footnote
In hyperaldosteronism secondary to CKD, advanced heart disease, or hepatic failure, PRA should be increased.
125
What are the **sensitive initial screening tests** for hyperaldosteronism?
* Plasma aldosterone-to-renin ratios (ARRs)
* Urinary Aldosterone-to-Creatinine Ratio (UACR)
## Footnote
These tests are used in both humans and cats suspected of having hyperaldosteronism.
126
True or false: A **single ARR** within the reference interval excludes PHA in cats.
FALSE
## Footnote
Measurement of a single ARR does not exclude PHA.
127
What is the **UACR** used for?
Reflects aldosterone secretion over time
## Footnote
Unlike blood tests, UACR does not require special handling and can be collected at home.
128
What is the **oral fludrocortisone** suppression testing protocol for healthy cats?
0.05 mg/kg q12h for 4 days
## Footnote
This protocol suppresses UACR by a median of 78% in healthy cats.
129
What is required for a **diagnosis of PHA**?
* Elevated PAC
* Identification of an AT
## Footnote
Histological confirmation of tumor type and resolution of clinical signs further confirm the diagnosis.
130
What is the **treatment of choice** for cats with a confirmed aldosteronoma?
Unilateral adrenalectomy
## Footnote
Surgery should be performed by experienced surgeons in a well-equipped facility.
131
What are common **perioperative complications** after adrenalectomy?
* Intraoperative hemorrhage
* Postoperative hemorrhage
* Acute kidney injury
* Thromboembolism
* Sepsis
## Footnote
Monitoring and management of these complications are crucial for recovery.
132
What medical treatment can be used for cats with PHA when surgery is contraindicated?
* Mineralocorticoid receptor blocker (spironolactone)
* K supplementation
* Antihypertensive drugs
## Footnote
Dosage adjustments may be necessary to control hypoK.
133
What is the **etiology** of PHA in dogs?
* Solitary adrenal adenoma
* Carcinoma
* Bilateral idiopathic adrenocortical hyperplasia
## Footnote
PHA is rare in dogs and usually occurs in middle-aged to older dogs.
134
What is the **clinical presentation** of sex hormone-secreting adrenal tumors in cats?
* Poor haircoat
* Dermal atrophy
* Cutaneous fragility
* Urine spraying behavior
## Footnote
Most cats with these tumors also have difficult-to-regulate diabetes mellitus.
135
What is the primary reason for measuring **sex hormones** in dogs suspected of having hyperadrenocorticism?
Cortisol concentrations below the reference range
## Footnote
Low cortisols may result from iatrogenic corticosteroid administration.
136
True or false: Elevated **sex hormone concentrations** can occur in many dogs without hyperadrenocorticism.
TRUE
## Footnote
Random, basal estradiol concentrations can exceed the reference range in individual dogs.
137
% of malignancy in IAGM?
14-30%
138
% of adrenal calcification in healthy old cat
33%
139
How many cats (%) can have PHA and plasma aldosterone concentrations in RR ?
25%
140
Medical treatment tried for feline sex hormone-secreting AT
Aminoglutethimide (inhibiteur desmolase CYP11A1 + aromatase: empêche androgènes-> estrogenes ) and trilostane
141
Equivocal adrenal asymmetry in AT: %
40%
142
What are the **clinically important members** of the Secretin hormone family?
* Secretin
* Glucagon
* Glucagon-like peptide (GLP)
* Gastric inhibitory peptide (GIP)
## Footnote
These hormones play significant roles in digestion and metabolism.
143
What is the primary action of **gastrin**?
↑ Gastric acid (H⁺) secretion
## Footnote
Gastrin acts synergistically with acetylcholine and histamine to stimulate gastric acid production.
144
What stimulates the release of **cholecystokinin (CCK)**?
* H⁺
* Fatty acids
* Amino acids
## Footnote
CCK is produced by I cells in the duodenum and jejunum.
145
What is the **core functional theme** of somatostatin?
Predominantly inhibitory hormone
## Footnote
Somatostatin inhibits gastric acid secretion, insulin secretion, and GI motility.
146
What initiates and coordinates **migrating motor complexes (MMCs)**?
Motilin
## Footnote
Motilin is released during fasting to clear the intestine.
147
What is the expected response of **secretin** in gastrinoma testing?
↑ gastrin release
## Footnote
In healthy animals, secretin does not change gastrin levels.
148
What are the **key actions** of GLP-1?
* ↑ Nutrient-induced insulin secretion
* ↓ Gastric motility
## Footnote
GLP-1 is the most potent insulin secretagogue and is evaluated for type II diabetes therapy.
149
List the **clinical signs** of NME.
* Nonspecific: Lethargy, Decreased appetite
* Dermatologic: Non-healing erosions/ulcers
* Possible autoimmune component
## Footnote
Lesion distribution includes lips, nose, ears, muzzle, paws, ventrum, inguinal region, and extremities.
150
What is required for the **diagnosis** of NME?
Hyperglucagonemia
## Footnote
Clinical signs of hormone excess and elevated serum glucagon levels are also considered.
151
What are the **common sites** for carcinoid tumors?
* Bronchial tree
* Lung
* Biliary system
* GI tract
* Other organs
## Footnote
These tumors secrete serotonin and kinins.
152
Gastrin: which cells secrete ? Physiologic stimulus ? Effect ?
G cells (antrum, duodenum); gastrin-34 major circulating gastrin; gastric distension and intraluminal peptides; acid and pepsinogen secretion; pancreatic enzyme secretion (acinar), trophic effect (gastric, intestinal, pancreatic tissue), stimulate mucosal blood Flow + antral motility
153
CCK; which cells secrete ? Physiologic stimulus? Effects?
I cells (duod, jej); CCK-33, CCK-39, CCK-58 GI effects, CCK-8 (neurons) peptide Nt in ENS; AA and FA in duodenum; H+; contraction GB (mediated via presynaptic cholinergic neurons), relaxation Oddi sphincter; pancreatic enzyme secretion (acinar cells) (in the presence of stimulatory level of secretin)(mediated via presynaptic cholinergic neurons), trophic effect on pancreas (growth), inhibit gastric emptying
154
Secretin: which cells secrete ? Stimulus? Effects?
S cells (duod prox); H+ in gastric juice, intraduodenal FA; stimulates secretion of bicarbonates and water (pancreatic ductal cells, duod), secretion of bile, inhibition of gastric secretion, gastric acid production, GI motility
155
GLP1; which cells secrete ? Stimulus; effects
L cells; intraluminal FA and glucose; stimulates insulin secretion in glucose-dependent manner; inhibits glucagon and gastric emptying.
GLP-2: upregulates glucose transporters
156
GIP; which cells ?, stimulus? Effects ?
K cells; nutrients in duodenum; insulin secretion (directly)
157
Somatostatin: which cells ? Stimulus ? Effects
D cells; nutriments (lipids and proteins), bile entering in the gut, inhibits acid and pepsinogen secretion, GB contraction, insulin and exocrine secretion, intestinal motility; decrease nutrient absorption
158
Motilin: which cells secrete? Stimulus ? Effects ?
M cells (duodenum distal, jejunum proximal); structurally related to grehlin; coordinates and initiate MMC (phase III propulsive) during fasting, coordinates gastric, pancreatic and biliary secretions during feeding
159
Ghrelin: which cells secrete ? Stimulus? Effects ?
P/D1 cells (stomach); structurally relater to ghrelin; nutrients (proteins); modulate GH (pituitary), increase gastric emptying, stimulate MMC, stimulate appetite and adipocyte growth. Link between dietary nutrients, calorie energy and pituitary-GH axis = vital for growth regulation
160
Serotonin; which cells secrete ?; effects
Enteric neurons and enterichromaffin like cells; stimulate contraction of GI smooth muscle; stimulate intestinal secretion
161
AB disorders in gastrinoma
Hypochloremic metabolic alkalosis
162
Zollinger-Ellison syndrome
Gastric antral hypertrophy (outflow tract obstruction described), hyperacidity, ulceration
163
Other hormones may be secreted by gastrinoma
Description of ACTH and insulin secretion
164
Diagnostic gastrinoma
US (pancreatic mass ou masses), basal serum gastrin concentrations/gastric pH (exclude before other causes of hypergastrinemia), provocative test with secretin (IV 2 U/kg secretin, 2-fold-increase 2 to 5 min post-injections, not True in all dogs); provocative testing with calcium (max gastrin detected at 60 min, 2-fold increase in serum gastrin concentrations)
165
% of metastasis in gastrinoma
85% at diagnosis: LN, mesentery, peritoneum, spleen and/or liver
166
What effect of gastrin on intestinal absorption ?
Inhibition of intestinal water absorption by gastrin ==> diarrhea in gastrinoma
167
Which other endocrine disorders are associated with gastrinoma in dogs ?
Adrenal hyperplasia and thyroid carcinoma
168
Clinical signs possible of glucagonoma in dogs
Lethargy, decreased appetite, signs of DM, and possibly Necrolytic Migrant Erythema (NME): crusting and rash with non-healing skin erosions and ulcers: especially mucocutaneous sites (AI ?): lips, nose, ears, muzzle, paws, ventrum, inguinal region, extremities
169
Diagnosis of glucagonoma in dogs ?
- US: not all pancreatic mass detected (CT more accurate ?)
- Hyperglucagonemia: 1,5-15 times the upper limit of RR; no cut-off in dogs; high serum glucagon with consistent clinical signs
- Measurement of plasma AA: lower plasma AA: in all dogs reduced concentrations of arginine, histidine and lysine
170
Definition of carcinoid tumors and tumor sites
Neuroendocrine tumors secreting serotonin or kinins; but in dogs and cat mainly non functional; sites: bronchial tree, lung, biliary system, GI tract (all). In cats: liver, pancreas, GI tract
171
Carcinoid syndrome
Watery diarrhea, abdominal cramps, bronchoconstriction, facile erythema
Report in 1 dog
172
173
% of unilateral PCC, local invasion and metastasis
Average diameter 5cm, >90% unilateral, 66% local invasion (56% vcc), 20% metastasis. No association between tumor size and vascular invasion
174
Which enzyme of catecholamine synthesis is stimulated by cortisol ?
PNMT: phenylethanolamine-N-methyltransferase
175
Which enzyme is the rate-limiting in the catecholamines synthesis ?
Tyrosine hydroxylase (tyrosine->DOPA) ==> inhibited by end products
176
Simplified synthesis of catecholamines
Tyrosine (tyrosine hydroxylase) => DOPA => dopamine => Norepi (PNMT) => epi
177
Which enzyme catalyze catecholamine metabolism ?
MAO= monoamine oxidase ; COMT= catechol-O-methyltransferase
178
Metabolites of catecholamines, and particularity of secretion
Epi=> metanephrine; Noepi=> normetanephrine
==> VMA vanillylmandelic acid
Catecho secretion: episodic (sympathetic preganglionic nerve fibers) ; metabolites: continuous secretion
179
180
Healthy chromaffin cells secrete preferentially? Vs PCC ?
Healthy: epinephrine ; PCC: norepinephrine
181
182
Which genes with high mutation in PCCs PGLs in dogs ?
SDH genes (SDHB and SHDH)
Associated with high malignancy in human
183
Signs of PCC in dogs
Paroxysmal episodes, dogs appears healthy between peak of catecholamines. Non specific signs: lethargy, weight loss, anorexia, vomiting. Also panting, collapse, seizures, sudden death due to arrhytmia. SHT (50%), seizures (CNS bleeding due to SHT and/or catecholamines-induced vasospasms), PU/PD (20%), hemoabdomen (retroperitoneal hemorrhage)
184
% of SHT and PUPD in PCC
50% and 20%
185
% of dogs with PCC with a second endocrine or neuroendocrine tumor
50%
Often coexistence with PDH, AT secreting cortisol
186
Diagnosis of PCC using urine/plasma normetanephrine
Better to use 2-3 times the upper limit of RR
UNCR > 97.4
PN> 3.6 nmol/L
187
Phenoxybenzamine
Non competitive, non selective, long-acting alpha-adrenergic blocker which covalently binds to alpha-1 and alpha-2 adrenoreceptors
188
If phenoxybenzamine not sufficient in PCC to stabilize catecholamine-induced complications
Add a selective beta 1-blocker (atenolol) (no non selective as pronalolol). Caution: not before phenoxybenzamine ==> risk of severe SHT
189
Prevalence of HS in DM
26%
20-33% (1 on 5 to 1 on 3)
190
Prevalence HS in CMH
6,7%
2-16%
191
PPV IGF-1 > 1000 ng/mL (131 nmol/L ?
95%
192
Diabetic cats with IGF-1 >1000 ng/mL; algorithme CT and MRI?
85% CT positive
15% CT negative:
- 50% MRI positive
- 50% MRI negative:
- 25% necropsy: pituitary normal
- 75% necropsy: 75% pituitary hyperplasia
193
Untreated DM cats, % false negative IGF-1 ?
9%
==> to be secreted IGF-1 needs portal insulin ==> insulin deficiency possible in newly DM diagnosed cats
194
% improved DM control,% DM remission after hypophysectomy and recurrence
71% of remission
95% improved DM control
12% of recurrence after a median of 248 days
IGF-1 marker of treatment success: postoperative 4-week IGF-1 nadir significantly lower in cats achieving DM remission
195
196
197
% of cats with long lasting injection of pasireotide enter in remission ?
25%
198
Gene pituitary dwarfism in GSD
LHX3
Recessive mutation
199
2 tests to confirm congenital GH deficiency
1) GHTH stimulation test (1mcg/kg)
2) alpha-adrenergics drugs: clonidine (10 mcg/kg) or xylazine (100 mcg/kg)
3) ghrelin 2 mcg/kg
Samples: immediately before, 20-30 after stimulation. Healthy dogs: 2 fold increase in GH concentrations
For ghrelin: GH > 5 mcg/L => exclusion of pituitary dwarfism
200
201
Treatment of canine pituitary dwarfism and AE
1) porcine GH 0,1-0,3 IU/kg SQ 3 times per week. AE: DM
2) progestins: SQ medroxyprogesterone acetate (2,5-5 mg/kg) 3 weeks-interval then 6 weeks-interval. Proligestone.
AE: pruritic pyoderma, skeletal malformations, mammary tumors, acromegaly, DM, cystic endometrial hyperplasia
3) levothyroxine if secondary hT4
202
203
Preprovasopressin includes?
Vasopressin, neurophysin-2, copeptin
204
Actions of AVP on endothelial V2 receptors
Release vW factor, tissue plasminogen activator, increase synthesis of NO and circulating concentrations of factor VIII
205
Actions of AVP on V1a receptors
Stimulates vascular smooth muscle contractions, platelet activation, hepatic glycogenolysis and gluconeogenesis
206
Actions of AVP on V1b receptors
Stimulates ACTH release and increases insulin or glucagon release from pancreas
207
% of CDI after head trauma in dogs, hypophysectomy dogs vs cays
7% of hypernatremia after head trauma in dogs
Transient CDI in 53 % of dogs after hypophysectomy (>2 weeks), permanent CDI in 22%
208
Why use of thiazides can help in NDI ?
Decrease Na absorption in distal renal tubules => diuresis => decreased blood Flow and GFR => increase Na and water reabsorption in PCT => reduction in water loss
+ tubuloglomerular feedback response-mediated reduction in GFR + upregulatory effects on AQP-2 and distal renal Na transporter expression
Other drugs:
- NSAID (to decrease renal blood flow and GFR)
- Sulfonylurea antidiabetic drug chlorpropamide: antidiuretic action: upregulate AVP ?
209
PHPT in dogs causes
87% adenoma, 8% hyperplasia, 5% carcinoma.
More than 1 gland involved < 10% of cases
210
Why NaCl 0,9% fluid of choice to fight hypercalcemia ?
Because Na+ compete with Ca2+ to reduce tubular reuptake
211
ECG abnormalities in hyperkalemia
Short-to-absent p waves, prolonged P-R interval, wide QRS complex, short R waves, tall T waves, premature ventricular complexes
212
% decline in insulin sensitivity for each kg of excess BW
30%
213
Ideal diet for diabetic obese cats
Carbonhydrates < 12-15 % ME
Protein > 40% ME
214
Stimuli for GH secretion in cats and inhibitors
Stimuli: GHRH, alpha-adrenergic agonists, ghrelin
Inhibitors: beta-adrenergic agonists, IGF1, somatostatins, dopamine receptor 2 agonists
No alteration in secretion of GH in cats
215
216
3 dermatologic signs associated with acromegaly
thickened myxedematous skin with
- excessive skin folds
- hypertrichosis
- thick hard claws
217
Side effect of the combination of digoxin and GC?
hypokalemia
ECVIM 2026
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