Week 6 Flashcards
(171 cards)
1
Q
What are the three clinically important lipids?
A
- Triglycerides- most common form of stored energy in mammals, derived from either dietary sources or endogenous hepatic production
- Cholesterol- the main sterol in animal tissues
- Fatty acids- these are relatively simple and important components of other lipids
2
Q
What are sterols?
A
also known as steroid alcohols, are a subgroup of the steroids and an important class of organic molecules. They occur naturally in plants, animals, and fungi, with the most familiar type of animal sterol being cholesterol.
3
Q
Why are cholesterol and triglycerides transported as macromolecular complexes? What are they called?
A
Because lipids are insoluble in water, they cannot be transported in aqueous solutions such as blood plasma. The macromolecular complexes are called lipoproteins.
4
Q
What is the structure of a lipoprotein?
A
Spherical structures consisting of a lipid core (triglycerides and/or cholesterol esters) and an amphophilic outer layer of phospholipids, free cholesterol and proteins.
5
Q
How are free fatty acids transported?
A
Bound to albumin
6
Q
Why is hydrolysis?
A
The cleavage of chemical bonds by the addition of water. For example, carbohydrate is broken into its component sugar molecules by hydrolysis, e.g. sucrose being broken down into glucose and fructose
7
Q
What are chylomicrons? What is the process by which they form? Where do they go??
A
* Following digestion, hydrolysis products (mainly fatty acids and monoglycerides) are converted to triglycerides in the intestinal mucosa cells–> then combined with phospholipids, cholesterol, and apolipoprotein to form CHYLOMICRONS. Chylomicrons are transported to the LIVER (and other tissues)
8
Q
Endogenously produced triglycerides and cholesterol are transported from what organ, in what form?
A
Endogenously produced triglycerides and cholesterol are transported from the liver as very low density lipoproteins (VLDL) and cholesterol transported also as LDL.
9
Q
What causes triglycerides to be released?
A
The activity of lipoprotein lipase, an enzyme located on the endothelium in many different tissues, for uptake as free fatty acids into e.g. fat or muscle
10
Q
What facilitates the uptake of triglycerides from chylomicrons into the liver?
A
Hepatic lipase on the endothelium of the liver sinusoids
11
Q
What causes the release of fatty acids? And where do they go? How are they transported?
A
Fatty acids are released from stored triglycerides in fat cells by the action of hormone sensitive lipase, under sensitive regulation by hormones.
The fatty acid are transported to the LIVER as non-esterified fatty acids (NEFA) bound to albumin
12
Q
What is the funtion of insulin?
A
* Promotes the esterification (storage) of glycerol and free fatty acids into triglycerides within adipose tissues.
* Insulin also increases the activity of lipoprotein lipase located on the endothelium of capillaries of extrahepatic tissues, promoting the movement of fatty acids into adipose tissue
13
Q
Thyroid tumours in dogs vs. cats
A
Dogs = carcinoma, poor prognosis
Cats= benign, good prognosis
14
Q
What are Heinz bodies?
A
Oxidatively damaged Haemoglobin
15
Q
A
Heinz bodies- could indicate hyperthyroidism
16
Q
What changes will we see on haemogram (CBC) for hyperthyroidism?
A
17
Q
What changes will we see for serum biochemistry related to liver enzymes in hyperthyroidism?
A
18
Q
What changes (not related to liver enzymes) will we see in serum biochemistry with hyperthyroidism?
A
19
Q
What is the initial test of choice for hyperthyroidism?
A
20
Q
What are the options if the TT4 is within reference interval but hyperthyroidism is still suspected based on clinical signs and base-line testing?
A
21
Q
Why is T4?
A
Thyroxine
22
Q
Total T4 vs. Free T4
A
* TT4 bound to protein
* T4= free T4= < 1%
23
Q
What is important to remember with cats and hyperthyroidism and renal function?
A
24
Q
Hypothyroidism occurence in dogs and cats
A
25
Clinical signs of hypothyroidism
26
Changes on haemogram (CBC) with hypothyroidism?
27
Target cells- may be suggestive of hypothyroidism
28
Clinical pathology abnormalities seen with hypothyroidism
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What is key when testing for hypothyroidism?
Serum total T4 (TT4)- basal level is usually low in hypothyroidism (standard and useful screening test BUT: not sensitive and not specific)
\* Just seeing a drop in T4 is not definitive
\* need a good history as some drugs can drop TT4 levels too
31
When testing for hypothyroidism, what will you find?
\*\* need to do a TT4, free T4, and TSH
32
Why don't you just use free T4 test for hypothyroidism?
A lot of false positive. Good at eliminating non hypothyroidism. Must do a combination in this case since all three tests lack sensitivity and specificity
33
Screening for lymphocytic thyroiditis (early hypothyroidism). Beneficial or not?
Questionable.
34
What tests should you run when you suspect hypothyroidism?
35
What are you measuring when you measure calcium?
36
What cells make PTH? Purpose? What cells produce calcitonin? Where? What does it do?
37
Hypercalcaemia DDXs
HARDIONS
38
Primary hyperthyroidism causes what in older dogs? Clinical sigsn and physical exam findings? Lab findings? What is key about PTH??
39
Why does hypercalcaemia cause PU/PD?
40
What is one of the more common causes of hypercalcaemia?
41
What are lab findings in hypercalcaemia caused by renal failure? Species differences between horses vs. dogs and cats?
42
What happens with calcium levels with renal secondary hyperparathyroidism?
43
What can cause vitamin D toxicosis, what are lab findings?
44
What is the most common cause of hypercalcaemia in dogs and cats?
45
DDX for hypocalcaemia
46
What is the first thing you do if you have hypocalcaemia? Why?
Check albumin levels
47
Why is it no longer recommended to correct for total calcium for hypoalbuminaemia in dogs?
48
Causes of hypoparathyroidism? Clinical signs? Lab findings?
49
What are the two types of secondary hyperparathyroidism?
50
What is the pathogenesis of nutritional secondary hyperparathyroidism in horses?
51
Why is hypocalcaemia seen with pancreatitis? Parturient paresis and eclampsia?
52
Why is hypocalcaemia seen with ethylene glycol toxicity?
53
Why is hypocalcaemia seen with hypomagnesaemia? What is spurious hypocalcaemia?
\* spurious hypocalcaemia: EDTA contamination of sample- the levels would be so low, the animal would not be alive
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Actions of insulin at the adipocyte
57
Link between glucose and fat metabolism
Insulin is at the heart of it
\* if the body has plenty of glucose, then it doesn't need to break down fat
58
What is hormone sensitive lipase (HSL)?
an intracellular lipase that is capable of hydrolyzing a variety of esters. In a stressed state you need energy, fat loss. A lot of hormones acting different ways on the HSL. Opposing insulin.
59
What are the four hormones produced by fat cells and macrophages in adipose tissue?
60
What is leptin?
\* effect on feeling of satiety and therefore appetite, dampens appetite and restricts feeding (if you're fat--\> do not need to eat as much)
\* link with reproductive activity stimulated with leptin, ties into metabolic rate and immune function
\* animals that do not have enough leptin- appetite is not switched off. But when measured in fat animals, often leptin is not low. Responsiveness of hypothalamus is decreased. "LEPTIN RESISTANCE"
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What are some adipokines?
62
What are the causes of obesity?
63
Consequences of obesity
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Visceral vs. subcutaneous fat
\* in the mesentery and in the abdomen, draining blood vessels straight to the liver- suddenly a lot of fat breakdown products--\> liver will bear the brunt of this metabolic activity
\* different hormones released by visceral vs. subcutaneous fat
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Why is obesity a chronically inflammatory state?
66
What is insulin resistance?
67
Why does type II diabetes mellitus result?
Obesity--\> Excess insulin production--\> eventually the pancreas may become exhausted
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Carbohydrate metabolism in peripheral insulin resistance
Most blood glucose shunted to the liver--\> involved in fatty acid production--\> build up of triglyceride build up--\> exacerbate obesity (fatty liver)
69
What is equine metabolic syndrome?
\* reason- originally from areas with sparse grass- they are not used to lush grass-- natural propensity to produce a lot of insulin.... called epigenetics (underlying predisposition and in an environment with way too much carbohydrates)
\* regional adiposity: animals with EMS often exhibit regional adiposity, laying down fat in areas such as the nuchal crest, behind the shoulders and around the tail region.
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Prevention of obesity
\* restrict carbohydrates (low glycaemic index) to restrict insulin production
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Hyperlipidaemia
\* Increased plasma triglycerides (\> 150 mg/dl) and/or cholesterol (\>30 mg/dl)
\* Primary (min schnauzers; briards)
\* Or secondary to various conditions, including endocrine diseases: diabetes mellitus, hyperadrenocorticism, hypothyroidism
\* consumption of fatty meal; severe obesity
\*\* milky plasma= triglycerides
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Mechanisms of Hyperlipidaemia
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Consequence of Hyperlipidaemia in ponies and donkey's
When suddenly nutrient deprived-- negative energy balance- has to mobilizes fat OR mare in late pregnancy OR lactating. Some major change in balance of nutrients coming and nutrients being used up.
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Consequence of negative energy balance in obese individuals
\*Metabolic rate slows to decrease consumption of glucose
\* Glucagon secretion increases and insulin secretion decreases
\* Gluconeogenesis, glycogenolysis and peripheral lipolysis
\* Shift towards using fatty acids as a primary energy source
\* Release of leptin is also increased
\*Physiological stress (illness, surgery, etc.) causes cortisol and catecholamine levels to rise, upregulating HSL activity and lipolysis
\* Excessive NEFA levels overwhelm the liver's capacity to process (limited ability to convert fatty acids into ketone bodies in the horse)
\* Triglyceride levels build in the liver and blood
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Treatment and Prevention of hyperlipidaemia
76
Which is usually primary and which is secondary in PU/PD?
polyuria is normally primary and polydipsia is normally secondary i.e. increased thirst occurs to compensate for the increased urine production
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What is the definition of polyuria?
increase urine volume- guideline: daily urine output \> 50 ml/kg
78
What is polydipsia?
Increased water consumption- guideline: daily fluid intake \> 100 ml/kg
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What is isothenuria? hyposthenuria? hypersthenuria?
\* urine with an osmolality equal to that of plasma - USG 1.008- 1.012
80
Difference between polyuria with urinary incontinence and pollakiuria?
\* polyuria- increased amount
\* urinary incontinence- involuntary leakage- not necessarily an increase in volume or amount
\* pollakiuria- increased frequency (small amounts often)
81
Expected usual range of Urine Specific Gravities of cats, dogs, and large animals
\*\* dog has a larger range than cats and large animals
\* a cat that is not concentrating- much more cause for concern than a dog
82
Cat, dog, horse, cow, sheep & goats normal water intakes and urine outputs
83
What balances blood pressure and water balance?
1. RAAS
2. hypothalamus
3. pituitary gland
\*\* These are the mechanisms that do not work in PU/PD-- ADH, renal tubules that respond to ADH and make the aquaporin channels, need medullary interstitium to be hypertonic, nephron population functional
84
Nephron concentration of urine
85
Mechanisms of primary PU and primary PD?
86
How does Central Diabetes Insipidus cause PU/PD?
87
What is Primary Nephrogenic Diabetes Insipidus?
88
What is secondary Nephrogenic Diabetes Insipidus?
89
Osmotic Diuresis
90
How do you get PU/PD with medullary washout?
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Primary polydipsia
92
Clinical approach to PU/PD
93
Does Max have polydipsia?
Yes
94
What does the urinalysis tell us about the causes of PU/PD?
95
What does a CBC, biochemistry tell us about the possible causes of PU/PD?
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97
What further testing other than CBC, biochem, and urinalysis would you conduct?
98
What is the last result with testing if unsure of cause of PU/PD?
99
What is the only type of biologically active Calcium?
Free calcium that is in the extracellular fluid (ECF) (skeletal muscle has nothing to do with regulation of calcium-- that is intracellular plasma within the sarcoplasmic reticulum)
100
Why is calcium important?
\* Enabling clotting factors: thrombin, factor X, factor Va to bind to anionic phospholipids on platelets surface-- without platelets we don't get clotting
\* NMJ activity: Calcium also enters the presynaptic terminal and causes vesicles to release their neurotransmitter, ACh from the synaptic vesicle into the presynaptic cleft
\* If we decrease calcium, we get over excitability of nerves and muscles-- too much calcium = lethargy (because hypocalcaemia lowers the threshold that the AP has to reach)
\* excitation contraction coupling in cardicac and smooth muscle
\* Calcium entry into secretory cells triggers release of products by exocytosis, for example insulin release
\* tight junction maintenance
101
What is excitation contraction coupling dependent on?
Extracellular calcium
102
Where does the body get calcium?
\* Diet- most passes straight through-- dependent on hormonal input
\* Skeleton-- 99% in bone and teeth (the rest is intracellular 0.9%)-- the most important source ECF is only 0.1% of the body (only for emergencies!!)
103
Hormones associated with regulation of calcium?
\* vitamin D
\* PTH
\* Calcitonin (emergency release mostly)
104
What is parathyroid hormone?
\* peptide hormone secreted by parathyroid gland
\* overall effect is to increase Ca++ in plasma
\* actions on bone, kidneys, and intestine
105
Important actions of PTH
\* increase blood calcium
\* increase urinary excretion of phosphorous
\* increases reabsorption of calcium
\* increase osteolysis and numbers of osteoclasts
\* increase rate of skeletal remodelling
\* activate adenylate cyclase
\* accelerate formation of active vitamin D
106
Calcitonin
\* secreted by C cells of thyroid
\* secretion is increased in response to elevated blood Ca++
\* can inhibit action of PTH on bone
\* antagonistic with PTC
\* emergency response to: hypercalcaemia & protect maternal skeleton during pregnancy
107
How do we release calcium from the bone?
\* Bone remodelling: mechanical engineering of the skeleton (as animal gets older and heavier), maintenance of plasma calcium
\* Rapid
- activate membrane bound calcium pumps of the osteocytes
- diffusion of calcium from bone fluid into plasma (therefore doesn't affect the integrity of bone)
- most important under normal conditions
108
Response to chronic hypocalcaemia
\* PTH mediates exchange between mineralise bone and ECF in two ways
1. increase in osteoclast formation
2. transient inhibition of osteoblasts
- still no effect on skeletal integrity (if it corrects the calcium balance)
- longer periods can result in cavity formation in the bone
109
How does PTH affect kidneys and intestinal function?
\* PTH enhances reabsorption of calcium
\* enhances activation of vitamin D by kidneys
- active vitamin D increases intestinal absorption of Ca++ (indirect effect of PTH)
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Negative feedback regulation of Ca++
111
Calcium sensing receptor
\* G protein coupled receptor family
\*\* widely distributed
112
Vitamin D and Calcium
\* Increases Ca++ absorption in the intestine
\* hormonal characteristics of vitamin D
- produced in skin from a cholesterol like precursor upon exposure to sunlight
- released into blood to act on distant target tissue
\* Activated via two sequential additions of an -OH (hydroxyl) groups
113
Activation of vitamin D
114
PTH and Vitamin D
115
Lactation and Ca++ demand
116
Situations where there are abnormally high demand for Ca++
\* Egg laying in birds- shell formation requires 8-10% of total body Ca++ per day
- specialized medullary bone
\* Start of lacatation
- large quantities of Ca++ transferred to milk
- decrease in Ca++ results in increase in PTH
- Plasma Ca++ normalised through increased intestinal absorption and bone resorption
117
What happens with PTH hypersecretion?
\* Bones, stones and abdominal groans
- response to Ca++ poor diets
- reduced excitability of muscle and nerves
- thinning of bones, skeletal deformities and increased fracture risk
- increased incidence of kidney stones
118
What happens with vitamin D deficiency?
\* impairment in intestinal absorption
\* PTH maintains plasma Ca++ at the expense of bones
- Rickets (pre puberty)
- Osteomalacia (adults)
119
What is milk fever?
\* Hypocalcaemia
\* Colostrum contains high levels of Ca++ (2g/L)
\* Requires 3 g per hour to produce the colostrum
\* results from inability to mobilize adequate Ca++--\> drop in circulating Ca++ which leads to restlessness, anxiety, anorexia, uncoordination and lack of interest in calf, progression to second stage without intervention.... coma
\*\* calcium gluconate infusion
\* can occur in sheep & dogs (but different response: excitement, restlessness, panting, trembling, muscular tetany and convulsive seizures, especially in small breeds of dogs during lactation)
120
Calcitonin is only important in certain situations (more emergency)
121
Hormones secreted and feedback mechanisms of the thyroid gland. Which is more potent?
122
What are the effects of thyroid hormones?
\* Increased metabolic rate
- resting energy expenditure
- protein synthesis and catabolism
- gluconeogenesis, glycolysis, and intestinal glucose absorption
- lipolysis
\* Stimulates growth and development (with growth hormone)
- particuarly neurological and musculoskeletal
\* Cardiac effects
- inotropic (agent that alters the force or energy of contractions) and chronotropic (changing nerves affecting the heart or rhythm of SA node)
123
Where might ectopic thyroid tissue be found?
Ventral neck, mediastinum, and heart base
\* may become neoplastic
\* common incidental finding
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What are the two types of hypothyroidism? Hyperthyroidism?
Hypothyroidism: congenital or adult onset
Hyperthyroidism: neoplasia, nodular hyperplasia
125
What is Cretinism?
Severly stunted growth due to hypothyroidism.
\* Common in lambs, sporadic in other species (weak or stillborn)
\* Disproportionate dwarfism, spinal kyphosis (hunch back)
\* Neurological impairment (dull and apathetic, ataxic gait)
\* Retain juvenile hair coat (thin, fine hair)
126
Adult onset hypothyroidism
\* Common in dogs, rare in other species
\* Vague and insidious course
\* Decreased metabolic rate: mental dullness, exercise intolerance, cold intolerance, weight gain
\* Alopecia- due to lack of thyroid hormone inhibiting anabolic stage of hair growth--- eventually it is bilateral alopecia, patchy at first
\* Hyperkeratosis and seborrhea (greasy and scaly skin)
\* Hyperpigmentation
\*Secondary infections (pyoderma, demodex, otitis externa)
\* Myxoedema (non-pitting oedema) due to mucin deposition in the skin especially around the face, limbs too. GOOD differentiator between hyper A
\* Infertility
\* Neuropathies: hindlimb paresis, megaoesophagus, myxoedema coma (nerves affected to the oesophagus for example)
\* Hyperlipidaemia: atherosclerosisf (at depositing in blood vessel walls), corneal lipidosis (lipid in the cornea)
127
Causes of Hypothyroidism
\* Loss of thyroid tissue: \*\*thyroid apalasia/ hypoplasia (bilateral)-- if you only have one side, no big deal- one can carry the load OR \*\*thyroid destruction (inflammation, neoplasia, iatrogenic) OR \*\*thyroid atrophy (impaired TSH/TRH secretion (rare) or idiopathic atrophy observed in dogs (may represent end stage thyroiditis))
\* Impaired thyroid function: \*\* defects in hormone synthesis, \*\* iodine deficiency (common in sheep), \*\* iodine excess (oversupplementation-- it is being stimulated with TSH and TRH but it can't produce thyroid hormone), \*\* goitrogenic toxins (inhibit synthesis of thyroid hormone), \*\* typically associated with goiter formation- non-inflammatory, non-neoplastic thyroid enlargement, reflects impaired thyroid function with secondary hyperstimulation by TSH
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Hyperplastic goitre-- can also form papillary structures (so big they fold in on themselves)
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Hyperthyroidism (most common endocrinopathy in cats)
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Clinical features of hyperthyroidism
\* increased metabolic activity: weight loss, polyphagia, hyperactivity/ irritability
\* skin: unkempt hair coat/ patchy alopecia
\* cardiac effects: arrhythmias, secondary hypertrophic cardiomyopathy, hypertension
134
Causes of hyperthyroidism
\* Nodular hyperplasia- multinodular goitre (aka), non-encapsulated proliferation of follicular thyroid, in cats may be functional (causing hyperthyroidism) or non-functional (incidental), sometimes seen in dogs and horses but typically non-functional (CAN BE REALLY SMALL- INVISIBLE TO THE NAKED EYE)
\* Thyroid neoplasia- less common- adenomas (well-defined soft solitary nodules), \*\*thyroid follicular carcinoma (aggressive tumours that metastasize readily via vascular invasion (more common in dogs than cats but typically non-functional)
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C cells- interstitial cells within the thyroid
\* Secrete calcitonin
137
Calcium homeostasis
138
Primary Hypoparathyroidism
\* Idiopathy- likely autoimmune
\* often transient because the parathyroid on the otherside will take some time to adjust but will eventually compensate
\* Deficiencies in PTH results in hypocalcaemia
\* Altered neuromuscular signal condution
- tremors/ tetany
- panting
- weakness/ recumbency
- arrhythmias
- seizures
139
Parturient hypocalcaemia
140
What is this? Causes?
Hyperparathyroidism
\* Primary hyperparathyroidism: uncommon, older dogs, caused by functional parathyroid neoplasm
\* Secondary hyperparathyroidism: caused by hypocalcaemia or phosphatemia
\* Secondary nutritional hyperparathyroidism: low dietary calcium or excess phosphates-- all meat diets (dogs, reptiles), high concentrate diet esp. brain (horses), high dietary oxalates (binds calcium)
141
Effects of hyperparathyroidism
142
Fibrous osteodystrophy
143
Pseudohyperparathyroidism
\* Humoral hypercalcemia of malignancy (HHM)
\* secretion of parathyroid hormone related protein (PTHrP) by some neoplasms
\*\* anal sac apocrine adenocarcinoma commonly do this
\*\* lymphoma (especially T cell)
\* Causes soft tissue mineralization: renal, gastric
144
"Rubber jaw"- pliable jaw due to bone resorption
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Endocrine pancreatic neoplasia
\* Insulinoma, Glucagonoma, Gastrinoma
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Endocrine pancreatic neoplasia
\*Generally malignant- often small and hard to see; metastasize along portal vein to liver
\* Classified by their hormonal profile: insulinoma (hypoglycemia), or gastrinoma (Zollinger-Ellison syndrome, Gastric hyperacidity and ulceration) or Glucagonoma (insulin resistance and secondary diabetes melitus, superficial necrolytic dermatitis)
\* gastrin is not normally something pancreatic cells secrete but they CAN
\*\* more often small and hard to see, by the time they get to a large size the animal is often dead
148
Superficial necrolytic dermatitis (hyperkeratosis on the foot pads, around the face, on the mouth)
Glucagonoma- insulin resistance and over time diabetes mellitus and/or superficial necrolytic dermatitis
149
Islets of Langerhan: glucagon (alpha cells), insulin (beta cells), somatostatin (delta cells), pancreatic polypeptide F cells
\* Richly innervated by both sympathetic and PS fibres
\* highly vascularized! Supplied by pancreatic artery and drain to portal vein
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151
What are the main sites of action of insulin?
1. Liver
2. Skeletal muscle
3. Adipose tissue
152
What is insulin? Half life?
Insulin is a peptide. 5-8 minute half life
153
Why is it important that insulin is released into the portal vein?
First pass effect
154
Regulating insulin secretion
155
Insulin secretion mechanisms
156
How is insulin activated?
insulin receptor has two chains alpha and beta.... tyrosine kinase receptor which phosphorylates when the receptor is activated by insulin binding. Activate insulin receptor substrate (family of molecules-- 6) allows enzymes to dock onto them.... which can activate other things which relate to the function of insulin. (from the blood--\> tissues e.g. adipose tissue-- so glut 4 transporters allowing glucose to come into the cell, hence dropping levels in the blood).
\*\* A family of molecules all switched on (500 mRNAs) following the binding of insulin to its target cell... via insulin receptor substrate
157
Insulin effect on liver
- insulin binds to receptor
- promotes storage of glucose as glycogen, as well as conversion of glucose to trigylcerides (glucose transporters are there normally- the level doesn't change which is different in muscle, for example)
\*\* Insulin switches on intermediary molecule called fructose 2 6 biphosphate--\> insulin leads to an increase in this molecule while glucagon leads to a decrease (COMPETITION)
\*\* switching off gluconeogenesis-- driving the pathway in a particular way
158
Insulin on muscle
1. upregulating glut 4 (instead of in the liver which activates glut 2 without upregulating)
2. Enhances conversion glucose to glycogen
3. Increases breakdown oxidation phosphofructokinase pyruvate dehydrogenase
4. stimulates the synthesis of protein in skeletal muscle and slows the degradation of existing proteins
\*\* glycolysis occuring within the muscle cell
\* trigger for insulin release is high glucose levels... when you stimulate glut 4 upregulated and insulin is taken up into the muscle
\*\* When exercising there are other ways to put glucose in the muscle cells-- not just insulin, but oxygen as well
159
Insulin on adipose tissue
\* glut 4 transporters
\* What is different? NO GLYCOGEN- no main storers
\* Very much driving glycolysis--\> making lipid droplets--\> differences relate to insulin.... lipoprotein lipase moves to the surface of endothelial cells. Enzyme present able to chop up LDL and release the fatty acids--\> the fatty acids can add to the formation of lipids in storage
1. Increases lipoprotein lipase (endothelium)- hydrolyses triglycerides to fatty acids and glycerol-- fatty acids to adipose tissue-- promotes esterification to triglycerides
2. Inhibits hormone sensitive lipase (triglycerides hydrolysed to free fatty acids) (insulin inhibits this particular hormone- no point in forming it and breaking it down the next second)
3. Glut 4 transporters increased
4. Increased triglyceride via glycolysis and alpha glycerol phosphate formation
160
Glucagon structure, function, stimulus for release, inhibition
\* peptide hormone
\* short half life
\* all of its action is at the level of the liver-- job is to start mobilizing the energy
\* Stimulus for release is low blood glucose or certain amino acids: arginine and alanine, gastrointestinal hormones, catecholamines
\*\* Inhibitors: high blood glucose, insulin, free fatty acids, somatostatin
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Molecular actions of glucagon
162
The relationship between insulin, glucagon, glycolysis and gluconeogenesis
163
Glucagon vs. Insulin key points
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Type I Diabetes Mellitus
165
Type II Diabetes Mellitus
166
Build up of proteins stopping the beta cells from functioning. in a CAT. Doesnt really occur in dogs.
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Major effects of diabetes mellitus-- diabete ketoacidosis
168
Diabetic coma causes
\*Acidosis OR
\* Dehydration-- glucose is getting peed out and water is going with it
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Acute Complications of hyperglycaemia and diabetes
170
Long term complications of hyperglycaemia
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What are the main 6 effects of insulin deficiency?
