Endocrine system & endocrine emergencies Flashcards
This insulin type is immediate acting with a short duration, making it ideal for constant rate infusions, and can also be administered IV.
a. Porcine zinc insulin suspension (Vetsulin®)
b. Regular insulin
c. NPH insulin
d. Glargine insulin
B
Somogyi phenomenom, episodes of hypoglycemia followed by rebound hyperglycemia, should be treated by:
a. increasing the patient’s insulin dose
b. administering insulin TID instead of BID
c. decreasing the patient’s insulin dose
d. administering insulin SID instead of BID
C
Which of the following is a typical abnormality seen with hypoadrenocorticism crisis?
a. Hyperglycemia
b. Hypernatremia
c. Hyperkalemia
d. Azotemia
C
The signs and symptoms of typical hypoadrenocorticism are caused by inadequate secretion of:
a. glucocorticoids
b. mineral corticoids
c. both glucocorticoids and mineral corticoids
d. anabolic steroids
C
What test is used to confirm a hypoadrenocorticism diagnosis?
a. Basal serum cortisol
b. Fructosamine level
c. Adrenocorticotropic hormone test
d. Metanephrine level
C
In hyperosmolar hyperglycemic states, sodium concentrations should be reduced at what rate?
a. >0.5^mEq/L/h
b. <0.5^mEq/L/h
c. >0.2^mEq/L/h
d. <0.2^mEq/L/h
B
Inadequate control of diabetes mellitus would be indicated by a fructosamine level of which value?
a. 225^μmol/L
b. 280^μmol/L
c. 360^μmol/L
d. 540^μmol/L
D
Which of the following is not a ketone?
a. Acetyl CoA
b. Beta-hydroxybutyrate
c. Acetoacetate
d. Acetone
A
The formula [2 × (Na + K)] + (BUN/2.8) + (glucose/18) calculates what value?
a. Base excess
b. Base deficit
c. Serum osmolarity
d. Anion gap
C
A serum sodium to potassium ratio (Na:K) of <27 is indicative of which disease process?
a. Hyperadrenocorticism
b. Hypoadrenocorticism
c. Diabetic ketoacidosis
d. Hyperosmolar hyperglycemia syndrome
B
What makes up the endocrine system?
Adrenal glands
Parathyroid
Thyroid
CNS
GIT
Pancreas
Kidneys
Gonads
Placenta
Neurotransmitters….
Act locally to control nerve function and are released by axon terminals of neurons into the synaptic cleft
Endocrine hormones….
released by “glands” into circulating blood and influence the function of the target cells
Neuroendocrine hormones….
secreted by neurons and influence the function of their target locations
Paracrine substances….
Secreted by cells into the ECF and affect the function of neighbouring target cells of a different type
Autocrine substances….
Secreted by cells into ECF and affect the same cells which produce them
Cytokines….
proteins secreted by cells into the ECF that affect the immune system and can function as paracrine, autocrine or endocrine hormones
Three broad classes of hormones
- Proteins & polypeptides i.e. insulin & glucagon
- Steroids i.e. cortisol, aldosterone & testosterone
- Tyrosine amino acid derivatives i.e. thyroxine, epinephrine, norepinephrine
How are all endocrine secretions controlled?
Tightly controlled through feedback mechanisms
Hormone receptor location
Large proteins that life on the surface or in the surface of cell membranes, cytoplasm or nucleus
What or how much a hormone exerts depends on
- Rate of production or secretion
- Availability if transport plasma proteins
- Ability of target tissue to convert the hormone
- Availability of the specific receptor
- Breakdown of the hormone
- Liver/Kidney ability to excrete
Hypothalmic-pituitary axis (HPA axis)
Hypothalamus co-ordinates the endocrine system. It releases corticotropin releasing hormone (CTRH) & other major hormones which is received by the pituitary gland causing the release of ACTH, GH, prolactin, LG, FSH. ADH is secreted from the posterior gland. The adrenal glands are signalled to release cortisol
Diabetes mellitus pathophysiology
Type 1 is insulin -dependent (congenital, immune-mediated, idiopathic) whereas type 2 is destruction of pancreatic b-cells (obesity, genetics, islet amyloidosis, abnormal insulin response). Approx. 50-70% of DM cases are type 1 and insulin-dependent
Secondary forms of DM
Pregnancy
Carbohydrate intolerance
Acromegaly
Cushing’s disease
Risk factors for DM
4-14y (peak 7-9y)
Females 2X as likely
Male neutered cats
General signs & symptoms of DM
Weight loss
PU/PD
Polyphagia
Glucosuria
Hyperglycaemia
Treatment of DM
Goal to eliminate clinical signs and resolve life-threatening hyperglycaemia & treat any concurrent disease
- insulin therapy (short or long acting)
- monitoring blood glucose and fructosamine levels
- dietary adjustment: high fibre, high complex carbohyrates, high protein
- glycaemic control: >80mg/dL
- exercise and weight loss
Why is a high fibre diet beneficial in DM patients?
Promotes weight loss and slows the absorption of glucose from the GIT which minimises the postprandial increase in glucose.
Somogyi effect
A too high administration of insulin results in periods of hypoglycaemia and rebound hyperglycaemia, release of glucagon, epinephrine, cortisol and GH. This results in an insulin resistance and a hyperglycaemia lasting 24-72h after a hypoglycaemic event
Treatment of somogyi effect
Decrease the insulin administration by 10-25%
DKA pathophysiology
Dysfunction of b-cells which result in absolute or relative deficiency of insulin. Insulin deficiency, diabetogenic hormone excess, fasting and dehydration lead to increased ketogenesis & gluconeogenesis. The liver is stimulated to produce glucose however cells are unable to utilise glucose due to a lack of insulin so fatty acids are converted into acetyl-CoA and further into the three ketone bodies: 1. Acetate, 2. acetoacetate, 3. b-hydroxybutyrate.
Diabetogenic hormone will enhance ketogenesis leading to ketonaemia and acidaemia.
Type of respiration associated with DKA or severe metabolic acidosis
Kussmal respiration
Risk factors and clinical signs of DKA
Diagnosed or undiagnosed DM
Dehydration
Weakness
Lethargy
Tachypnoea
Uraemic breath
Vomiting
Abdominal pain/distension
Plantigrade posture (cats)
Potential lab findings in patients with DKA
Severe uraemic acidosis (metabolic acidosis)
Lyte disturbances (K, Na, K, P)
Pre-renal azotaemia
Hyperlipidaemia
Haemoconcentration
Glucosuria, ketonuria, proteinuria
Ketonaemia
Leukocytosis
Increased liver and cholestatic enzymes
Potential ultrasound findings in DKA
Pancreatitis
Peritonitis
Hepatomegaly
UTI
Treatment of DKA
Main goals are to restore & maintain hydration, provide sufficient insulin, correct acidaemia & electrolytes, and treat underlying disorders.
IVFT: won’t decrease ketones but will reduce glucose and help correct dehydration
Insulin: usually regular insulin inititally after some time of rehydration
Electrolyte supplementation: K, Phos, Mg (if refractory hypokalaemia)
Bicarbonate: only if persistant pH <7
Glucose stabilisation & monitoring: reduce 50-100mg/dL/hr
Encourage eating: give anti-emetics etc as required
What cells make up the endocrine pancreas
a-cells: secrete glucagon
b-cells: secrete insuline
delta-cells: secrete somatostatin
f-cells: secrete pancreatic polypeptide
All regulate glucose production and utilisation
Hypoglycaemia signs
Lethargy
Ataxia
Coma
Weakness
Seizures/tremors
Death
Pupil dilation
Anxiety
Drooling
Neuroglycopaenia
Inadequate glucose concentration in the brain that affects the function of neurons altering brain function & behaviour.
(Severe neuronal damage -> reduction in ATP, cellular damage & oxidative damage)
Hyperosmolar hyperglycaemic state
Life-threatening emergency in patients with DM and is charatcerised by hyperglycaemia >600mg/dL and hyperosmolarity >350mOsmL, with dehydration and without a ketoacidosis.
Usually occurs when a DM patient stops drinking resulting in ongoing osmotic diuresis and PU resulting in significant free water deficit and increased osmolarity.
Serum osmolarity
(2 X (Na +K)) + (BUN/2.8) + (Glu/18)
Normal serum osmolarity for cats and dogs
Cats: 290-330
Dogs 290-310
Clinical signs of hyperosmolar hyperglycaemic state
Neuro signs
seizures
lethargy
weakness
hypothermia
anorexia
vomiting
death
Treatment of hyperosmolar hyperglycaemic state
Gradual rehydration 0.9% NaCl - replaces glucose with Na
Lower glucose to <250-300 by 50-75mg/dL/hr (not too rapid due to idiogenic osmoles)
Insulin therapy 0.025-0.05U/kg/hr (if too rapid drop in glucose drop insulin 25-50%
Address electrolytes (K, P, Mg)
Treat concurrent disease
Insulinoma….
Pancreatic b cell tumors that secrete insulin without regulation and are a type of amine precursor uptake & decarboxylation (APUD) -oma that are generally malignant.
Signs and symptoms of insulinoma
Hypoglycaemia
Weakness
Collapse
Weight loss
Treatment of insulinoma
Glucose administration (may be refractory)
Frequent meals (increased fat, fibre, carbs, AVOID simple sugars)
Glucocorticoids (glucagon 5-40ng/kg/min)
Ex-lap to remove tumor
Diazoxide
Somatostatin therapy (octreotide)
Prednisone
Hypoadrenocorticism pathophysiology
Inadequate secretion of glucocorticoids and mineralcorticoids by the adrenal cortex. It is usually due to bilateral adrenal atrophy with fibrosis and in most cases is immune-mediated. The primary mineralcorticoid which is deficient is aldosterone whilst the primary glucocorticoid deficient is cortisol & corticosterone.
Atypical Addison’s
Deficiency in ONLY glucocorticoid secretion
Cortisol
Regulates protein, carbohydrate and lipid metabolism, modulates immune function and ensures appropriate production of catecholamines
Aldosterone
Mineralcorticoid released from the Z. glomerulosa and part of the hormonal cascade that begins in the kidneys.
It also maintains normovolaemia and increased K excretion.
Signs & symptoms of hypoadrenocorticism
Weakness
Lethargy
Vomiting & diarrhoea
Weight loss
Anorexia
Trembling
PU/PD
Collapse
GI bleed
Signs of Addisonian crisis
Pallor
Tachycardia
Hypothermia
GI signs and haemorrhage
Hypoglycaemia
Hypotension
Hyperkalaemia
Risk factors for hypoadrenocorticism
Middle to old age
Female dogs
Std poodles, portugese water dogs, great danes, rottweiler, WHWT, wheaten terriers
Treatment of hypoadrenocorticism
Glucocorticoid therapy (hydrocortisone/pred/florinef/DOCP)
IVFT
Treatment of hypoglycaemia
Anti-emetics
GI protectants
Dexmethasone (won’t interfere with ACTH stim)
Treat underlying dz
Treat life-threatening bradyarrhythmia (due to high K)
AVOID nsaids
Lab findings with hypoadrenocorticism
ACTH stim
CBC: eosinophilia, NO stress leukogram
Blood smear: normocytic, normochromic anaemia
Biochem: pre-renal azotaemia & low albumin
Acid-base/electrolytes: metabolic acidosis, low Na + Cl, high K (Na:K <27:1), low glucose
Glucose
The breakdown product of carbohydrates and is an important energy source in the animal body
Glucose homeostasis
Balance between absorption, production & utilisation
How does glucose become available
Via intestinal digestion and absorption of carbohydrates, the breakdown of glycogen via glycogenolysis or the production of glucose from gluconeogenesis
Postprandial glucose is stored where as what?
Stored in the liver as glycogen.
Glycogen can be stored in any cell but mostly the liver and skeletal muscle
Major hormones which regulate glucose
Insulin (released as BG rises)
Glucagon, catecholamines, cortisol & growth hormone (released as BG decreases)
Glycogenolysis can sustain the body’s glucose demands for
6-12h
Gluconeogenesis
Produces glucose in times of prolonged or increased demand and involves using end-products of glycosis i.e. lactic acid, pyruvate, glycerol and amino acids to produce glucose
Cortisol role in glucose production
Helps to mobilise proteins and adipocytes to ensure amino acids and fatty acids are available for glucose production.
Also serves to inhibit the actions of insulin and potentiate effects of glucagon & epinephrine in the liver.
What percentage of amino acids in the body can be converted to glucose
60%
How much can the kidney contribute to total glucose production in circumstances such as hepatic insufficiency
40%
Glucose transporters required for glucose to enter brain cells
GLU-1 TO GLU-5
Treatment of hypoglycaemia
Buccal glucose limited effectiveness
IV Dextrose 50% 0.25-0.5g/kg dilute 1:3 (as req)
CRI IVFT + 2.5-7% D50
Glucocorticoids
Glucagon
Frequent meals
Monitor BG closely
2 most common reasons for hyperglycaemia
Diabetes mellitus and stress-induced
How does DM occur
Absolute or relative insulin insufficiency
Other reasons for insulin deficiency excluding DM
exocrine pancreatic insufficiency, pancreatectomy
Causes of hyperglycaemia
DM
Stress (catecholamine release)
Postprandial
Hyperadrenocorticism
Hypersomatotropism
Diestrus
Drugs (glucocorticoids, progestins)
Parenteral nutrtion
Fluids with glucose
Glucosuria
Glucose is filtered by the kidney with almost all of it being reabsorbed into the PCT thus glucosuria rarer unless BG >180mg/dL in dogs and >300mg/dL in cats
Clinical situations where insulin resistance occurs
Exocrine pancreatic insufficiency
Insulinoma
cortisol, epinephrine, GH or progesterone elevation (cushings, diestrus, high lipids, hypothyroidism)
Diabetogenic drugs
Insulin resistance
exerts a negative influence on insulin sensitivity at the level of the insulin receptor or the insulin signaling cascade resulting in altered carbohydrate metabolism, increased hepatic glucose production, impaired peripheral glucose utilisation and relative insulin insufficiency.
Adrenal cortex
Produce and secrete mineralcorticoids (glomerulosa), glucocorticoids (fasciculata) and sex hormones (reticularis) and are under the control of the juxtaglomerular apparatus.
Adrenal medulla
Produces and secretes catecholamines and is regulated by the autonomic nervous system
Pheochromocytoma
Catecholamine-producing tumors that predominantly arise from the adrenal medulla or extra-adrenal where they are neuroendocrine chromaffin cell tumors. They occur in 13-31% of all adrenal tumors.
Pheochromocytoma pathophysiology
Intermittent production of supraphysiological catecholamines cause clinical signs associated with high sympathetic tone (tachycardia, arrhythmias, hypertension). As the tumor progresses intravacular invasion or thrombus formation and ascites may occur.
3 layers of the adrenal cortex
Zona glomerulosa
Zona fasciculata
Zona reticularis
Pheochromocytoma clinical signs & PE
Weakness & collapse
PU/PD
Vomiting
Dyspnoea
Anorexia & weight loss
Seizures
Abdominal pain & ascites
Hypertensive crisis
Treatment of pheochromocytoma
Treat hypovolaemic shock
Antiarrhythmics
Treat hypertensive crisis
Control excessive catecholamine release (phenocybenzamine, a-antagonist)
Adrenalectomy
Hyperaldosteronism
Increased aldosterone either by increased autonomous secretion, decreased renal perfusion or excessive renin production.
Primary hyperaldosteronism
Due to hyperplasia or neoplasia and is due to autonomous secretion. This is the predominant cause in cats.
Treatment of hyperaldosteronism
Adrenalectomy (70-77% survival)
Hyperadrenocorticism (cushings)
Excess adrenal cortex hormone release (most cases glucocorticoid excess). Most produced in the zona fascicula and reticularis under the control of the anterior pituitary with the release regulated by ACTH.
Clinical signs of cushings
PU/PD
Polyphagia
Exercise intolerance
Muscle weakeness
Pot belly
Dermatological abnormalities (pyoderma, cutaneous atrophy)
Amount of the adrenal cortex that must be destroyed before apparent clinical signs
90%
Lab findings with hypercotisolism/hyperadrenocorticism/cushings
Thrombocytopathy
High ALP
High cholesterol
Hyperglycaemia
Low USG
Where are the adrenal glands located
Craniomedial poles of the kidneys
Treatment of hypercortisolism
Suppress glucocorticoid synthesis (trilostane)
Adrenalectomy (functional adrenal tumors)
1 test for diagnosing cushings
LDDST. Can do urine cortisol:creanine ratio
Most common form of hypoadrenocorticism
Primary, likely immune-mediated to all three layers of the adrenal cortex
Secondary hypoadrenocorticism
Uncommon and results from abnormal pituitary or hypothalamic function (lack of CRH). Can occur due to trauma and neoplasia. Mineralocorticoid levels are preserved whilst cortisol production is affected.
Aldosterone is vital to maintaining….
Normal sodium, potassium & water homeostasis at the site of the renal tubule. It also plays a role regulating the GIT as well as the salivary & sweat glands
Aldosterone deficiency
Causes increased sodium, chloride and water via the urine contributing to dehydration, prerenal azotaemia, unconcentrated urine, hypovolaemia, weakness & shock.
It also impairs GI sodium absorption leading to decreased chloride and water absorption from the GI lumen.
Marked hyperkalaemia may also occur and is exacerbated by decreased GFR.
Acidosis also occurs and shifts K out of cells -> cardiac arrhythmias
Glucocorticoid deficiency (low cortisol)
Leads to decreased intravascular volume, hypotension, and hypoglycaemia. Other: GI ileus, exacerbation of vomiting and diarrhoea.
History & clinical signs of hypoadrenocorticism
Waxing and waning signs that are responsive to IVFT & glucocorticoid therapy, and are usually triggered by a stressful event. Extremely rare in cats.
Vomiting & diarrhoea
Melena
PU/PD
Ataxia
Tremors/seizures
Anorexia & weight loss
Diagnosis of hypoadrenocorticism
Bilateral adrenal atrophy (can also be normal)
Microcardia, decreased pulmonary vessel vasculature, narrowed caudal vena cava (hypovolaemia)
Absence of a stress leukogram with variable WBC counts
Hyperkalaemia, low cholesterol, increased liver enzymes
Hyponatraemia (Na:K ratio <27:1; <20 VERY suggestive)
Azotaemia (prerenal) with inappropriate low USG
ACTH stimulation pre and post <2ug/dL (baseline cortisol <2ug/dL)
Hypoproteinaemia/hypoalbuminaemia
Hypercalcaemia
Metabolic acidosis
Primary v. secondary hypoadrenocorticism
ACTH stimulation cannot differentiate. In the face of electrolyte abnormalities is highly probable that it is primary and mineralocorticoid therapy will be required long term. Where there isn’t electrolyte abnormalities it is hard to determine whether primary or secondary. Endogenous plasma ACTH will differentiate as will be high in primary due to loss of feedback inhibition from cortisol on pituitary function and low if secondary.
Emergent treatment of hypoadrenocorticism
Shock: improve tissue perfusion, correct electrolytes, treat arrhythmias
Rapid IV glucocorticoids (dexamethasone or hydrocortisone)
Hyperkalaemia: mostly corrects with IVFT, calcium gluconate, dextrose, bicarbonate (if persistent low pH), tebutaline
* Cats can take 3-5 days before showing improvement
Long term therapy for hypoadrenocorticism
Fludrocortisone (mineralcorticoid) + pred (for glucocorticoid)
DOCP (only mineralcorticoid) + pred
Thyroid hormones
Critical in the regulation of physiological homeostatis: basal metabolic rate, many other body system functions.
Thyroid hormone secretion
Relies on thyroid-stimulating hormone released from the posterior pituitary under negative feedback of T3 & T4
Biologically active form of thyroid hormone
T3
Thyroid testing
T4 the most sensitive indicator of thyroid dysfunction as 90% of EC pool of thyroid hormones is T4.
Hyperthyroidism
Excessive thyroid hormone release and is mostly due to autonomous secretion due to hyperplasia or neoplasia.
Most common endocrinopathy of geriatric cats but rare in dogs
Hypothyroidism
Inadequate thyroid hormone production and results from decreased TSH stimulation or decreased production of thyroxine within the thyroid gland. Most often due to immune-mediated destruction of the thyroid and is most common in dogs but quite rare in cats.
Hyperthyroidism clinical signs
Reflect increased demands of excessive thyroid hormone
Polyphagia
PU/PD
Weight loss
Restlessness/altered behaviour
Vomiting & diarrhoea
Diagnosis of hyperthyroidism
Suspicion
Elevated thyroid values
Enlarged thyroid
Treatment of hyperthyroidism
Aimed at restoring normal thyroid hormone production
Methimazole
Iodide deficient diet
Thyroidectomy
Radioactive iodine deficiency
Hypertensive retinopathy
Most common reason for acute blindness in geriatric cats and is often permanent so should be treated immediately. Cats will have mydriasis, retinal haemorrhage and hyphema. It is treatment with amlodipine and +- acepromazine or hydralazine.
Thyroid storm
Rare consequence of uncontrolled hyperthyroidism and clinical signs reflect acute exacerbation of hyperthyroidism i.e. fever, cardiovascular, GIT and CNS signs. Treatment aims to decrease thyroid hormone production and decrease systemic effects of systemic thyroid hormones and identify underlying cause.
Iatrogenic hyperthyroidism
Either by over supplementation or ingestion of thyroid-containing offal.
Hypothyroidism clinical signs
Lethargy
Weight gain
Decreased appetite or stamina
Alopecia or ‘rat tail’
Seizures/vestibular disease
Stupor/coma
Diagnosis of hypothyroidism
Low TT4
Mild, non-regenerative anaemia
Hyperlipidaemia
Treatment of hypothyroidism
Levothyroxine
Myxedema coma
Due to severe, untreated hypothyroidism leading to hyaluronic acid accumulation in the dermis leading to skin thickening, weakness, bradycardia, hypothermia, coma or death. It is treated with supplementating thyroid hormone, resuscitating the patient and quickly identifying underlying disease.
Diabetes insipidus
Inadequate free water reabsorption in the kidneys causing polyuria. ADH is released from the posterior pituitary gland and acts on principal cells of the renal collecting tubules allowing electrolyte free water reabsorption in a normally water-impermeable region of the nephron. AVP/ADH released due to hyperosmolality or ineffective circulating volume and binds to V2 in renal collecting tubules activating G-protein and ultimately inserting specialised water channels into collecting tubule cell luminal membrane. They allow electrolyte free water to be reabsorbed from ultrafiltrate. Low AVP/ADH prevents this and large volumes of very dilute urine is produced, the animal drinks excessively to compensate.
Nephrogenic v. central DI
Inadequate free water reabsorption in the kidneys causing polyuria. ADH is released from the posterior pituitary gland and acts on principal cells of the renal collecting tubules allowing electrolyte free water reabsorption in a normally water-impermeable region of the nephron. AVP/ADH released due to hyperosmolality or ineffective circulating volume and binds to V2 in renal collecting tubules activating G-protein and ultimately inserting specialised water channels into collecting tubule cell luminal membrane. They allow electrolyte free water to be reabsorbed from ultrafiltrate. Low AVP/ADH prevents this and large volumes of very dilute urine is produced, the animal drinks excessively to compensate.
Nephrogenic v. central DI
Central due to pituitary disease and nephrogenic due to V2 receptor or aquaporin-2 channel issue.
Central: TBI, Neoplasia, pituitary surgery, ROSC, Inflammation, idiopathic, drugs
Nephrogenic: Paraneoplastic, hypercalcaemia, hypokalaemia, leptospirosis, ureteral obstruction, kidney failure, drugs
Clinical signs of DI
PU/PD
Hypernatraemia
Inappropriately low USG (isosthenuric or hyposthenuric), isosmolar urine
CNS signs: seizures, head-pressing, obtundation
Definitive diagnosis of DI
Exogenous AVP (desmopressin responsive >50% improvement in USG)
Modified water deprivation test (withhold water until 3% body weight loss, give exogenous AVP)
Treatment of DI
Water replacement: D5W
AVP adminisatrion: desmopressin
* Must monitor Na and avoid too rapid drop to avoid cerebral oedema
Acetyl-CoA synthesis
Either condensation or utilisation
Condensation: 2 ACA > acetoacetate > b-hydroxybutyrate and acetone
Utilisation: 3 ACA > acetoacetate > b-hydroxybutyrate and acetone
Ketone bodies use
Synthesised as an alternative energy source when intercellular glucose concentrations cannot meet the metabolic demands. Acetyl-CoA produced from b oxidation of fatty acids which is facilitated by low insulin and increased glucagon
Insulin protocols for DKA
0.2u/kg IM then 0.1u/kg IM one hour later
CRI 1.1-2.2U/kg/day
Add glucose to fluids to maintain BG, may need to adjust insulin CRI
Pathophysiology of HHS
Increased circulating counter-regulatory hormones (glucagon, catecholamines, cortisol and GH) in conjunction with relative or absolute lack of insulin > inhibition of insulin mediated glucose uptake (epinephrine and glucagon) leads to glycogenolysis and gluconeogenesis; cortisol & GH inhibit insulin activity > increased circulating glucose.
Diabetogenic hormones
Increased protein catabolism leading to impaired insulin activity and provides amino acids for hepatic gluconeogenesis
Corrected Na
Na is the main determinant for serum osmolality and in a state of hyperglycaemia as seen in HHS will mask the true Na concentration, so corrected Na:
Na(meas) + 1.6 (glu(meas)-glu(norm)/100)
Glucose in mg/dL
Sodium mEq/L
Glucagon
Secreted from pancreatic a-cells which stimulate the liver to perform glycogenolysis and gluconeogenesis to increase hepatic glucose production
B-cells of the pancreas
Secrete insulin in response to increased glucose, amino acids and intestinal hormones. This stops glucose formation, promotes glycogen storage, stimulates glucose uptake and utilisation, decreases glucagon secretion and promotes triglyceride formation in adipose tissue
Hypoglycaemia
Utilisation > production
1. Inadequate intake
2. Excessive utilisation
3. Dysfunctional glycogenolysis or gluconeogenic pathway
SIADH
Syndrome of inappropriate antidiuretic hormone
Hyponatraemia due to excessive ADH release from the neurohypophysis or other source (cerebral, pulmonary or medication)
Signs and findings of SIADH
Na <120mEq/L causing vomiting, CNS abnormalities, anorexia, arrhythmias. Osmolality usually <280mOsm/kg and urine osmolality >150mOsm/kg
SIADH Treatment
Discontinue fluid therapy
Restricted water access
HTS3% over 2-4 hours
Reduce Na <12mEq/L/day
Initial Na aim 125-130mEq/L
Low cortisol
Altered cellular function so affects; protein, lipid and carbohydrate metabolism, immunodysregulation, catecholamine & agremergic receptor function and dysfunctional cellular membranes > CIRCI
Calculate osmolarity for a cat with Na 140, K 4.0, BUN 30, Glu 450
(2x(140+4)) + (30/2.8) + (450/18)
= 323mOsm/L (normal 290-330)
Calculate osmolarity for a dog with Na 135, K 3.8, BUN 32.1, Glu 500
(2X(135+3.8)) + (32.1/2.8) + (500/18)
= 317mOsm/L (normal 290-310)
