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Bloc E - Digestion and metabolism > Endocrino > Flashcards

Endocrino Flashcards

1
Q

By which 2 systems the homeostasis is maintained?

A
  1. ANS
  2. Endocrine
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2
Q

What are the types of hornomes based on their sites of action?

A
  1. Endocrine: travels in the blood
  2. Autocrine: acts on the same cell
  3. Paracrine: acts on cells adjacent
  4. Neurotransmission: travels trough neurons
  5. Neuroendocrine: travels trough neurons and bloodstream
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3
Q

Which hormones are directly neurotransmitted to the pituiary gland?

A

Vasopressin and oxytocin through the posterior pituitary

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4
Q

Which hormones are received by the anterior pituiary gland via the PITUIARY PORTAL SYSTEM?

A
  • TSH
  • ACTH
  • LH
  • FSH
  • GH
  • PRL
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5
Q

TRH (Thyroid releasing Hormone) pathway?

A

TSH (Thyroid Stimulating Hormone) –> Thyroid –> Thyroid hormones

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6
Q

CRF pathway?

A

CFR –> ACTH –> Adrenal –> Cortisol

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7
Q

GnRH pathway?

A

LH (Luteinizing Hormone) & FSH (Follicle Stimulating Hormone) –> ovaries and testies –> sex hormones

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8
Q

GFR (stimulates) & somatostatin (inhibits) what?

A

GH (growth hormone)

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9
Q

Dopamine inhibits and stimulates what?

A

Stimulates PRL (prolactine) –>

  • Mammary gland (milk ejection during lactation)
  • Mother cannot have another child when lactating
  • Behaviour and uterine contraction during labour
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10
Q

Anatomy of the thyroid gland?

A
  • The Thyroid Gland is composed in the human of two functional cell lines of distinct embryological origin, the follicular cells, that constitute the bulk of the gland and are organized in a follicular architecture, and the so-called clear cells, which are located between the follicles.
  • The follicles contain “colloid”, largely composed of thyroglobulin, the protein in which thyroid hormones are synthesized and stored until they are released.
  • These cells produce calcitonin, which is involved in the regulation of calcium metabolism.
  • The thyroid is comprised of two separate lobes connected by an isthmus.
  • Goitre = big thyroid.
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11
Q

Main roles of thyroid?

A
  • In all vertebrates, thyroid is involved in development, growth and programmed functions
  • In all homoeothermic species (warm-blooded), thyroid is involved in thermogenesis and diet-induced adaptive thermogenesis, facultative thermogenesis and ancillary metabolic effects
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12
Q

Iodine uptake ​mechanisms?

A
  1. Synthesis: movement of iodine into the follicular cell (NIS + NAKatpase –> Pendride –> Follicule)
  2. Organification: cannot have iodide just floating around as it will destroy the cells, so we attach it to amino acids through organification
  3. Coupling: you take one thyrocyl residue and attach it to another thyrocyl residue and you get thyroid hormone
  4. Storage: once the hormone is produced, it is stored in the colloid via thyroglobulin (stored there until it’s needed (we have a huge reserve of this hormone, can be stored for 4-6 weeks!)
  5. Endocytosis: invagination of our volloid to form these colloid droplets containing the hormone
  6. Lysosome: digest the colloid droplets to release T4 (thyroid hormone), which is converted to T3 (active form more potent and abundant) in the body gland by the process of deionization T4 deionization ® T3
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13
Q

Organification, coupling, transport, recycling and storage of thyroid hormone?

A
  • The thyroid hormones are iodinated amino acids derived from the amino acid tyrosine. The two forms of thyroid hormone are tetraiodo-L-thyronine (thyroxine, abbreviated T4), and triiodo-L-thyronine (abbreviated T3) collectively referred to as thyroid hormone (TH).
  • T4 is transformed to T3 peripherally and in the pituitary gland by the process of deionization T4 deionization –> T3.
  • About 80% of circulating T4 is deiodinated either in the 5 or 5’ positions, about 35% being converted to T3, the rest to rT3.
  • T3 is about ten times more abundant than T4 at the nuclear receptor level and more potent
  • T3 is ultimately responsible for most of the activity of thyroid secretions
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14
Q

Regulation of Thyroid Function: Hypothalamic-Pituitary-Thyroid Axis?

A

TSH (glycoprotein) effect:

Earliest effect is on the release of preformed hormone

  • Tg endocytosis
  • Digestion and release of iodoaminoacids
  • Intrathyroidal deiodination of iodotyrosines

Stimulates all steps in the synthesis (except Pendrin)

  • NIS level and activity
  • I- oxidation and organification
  • Coupling of iodotyrosines
  • Tg synthesis and processing

Necessary for thyroid cell replication and differentiation

Cortisol, dopamine, cytokines and somatostatin can influence the plasma levels of thyroid hormone even if the hypothalamic-pituitary-thyroid axis is intact

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15
Q

Symptoms of Hyperthyroidism?

A
  • Cardiovascular effects: palpitations (direct effect on activation of calcium channel and indirect effect on SNS), exertion dyspnea, hyperdynamic precordium, wide pulse pressure (high systolic but low diastolic pressure), peripheral oedema, CHF and atrial fibrillation
  • Restlessness, anxiety and sleeplessness
  • Muscular weakness
  • Weight loss in spite of increased appetite
  • Profuse sweating and heat intolerance
  • Diarrhea
  • Eye changes
  • Goitre (increased size of the thyroid)
  • Rapid forceful heartbeat
  • Tremor
  • Dermopathy and acropachy
  • Can present like apathic hyperthyroidism because of down-regulation of SNS
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16
Q

Symptoms of hypothyroidisim?

A
  • M. MOOD- depressed
  • M. Mental processes slowed and poor memory
  • M. Muscular weakness and constant fatigue, tiredness
  • M. Mass, weight gain
  • M. Metabolic rate slowed, sensitivity to cold
  • M. Movements of bowels slowed, constipation
  • M. Myocardial Dysfunction
  • M. Maternity delayed, Menstrual irregularities
  • Neuropsychiatric symptoms (cognitive, ambition, hallucination)
  • Patient’s complexion is sallow (xantoderma)
  • The skin surface feels coarse, thick, non-pitting edema (myxedema)
  • Hair and nail changes
  • Delayed relaxation of deep tendon reflexes as a sign of active muscular dysfunction
  • Impaired intestinal motility (constipation) because of decreased parasympathetic activity
  • Cardiac disorders: LESS COMMON, CHF (uncommon), coronary heart disease, pericardial effusion
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17
Q

How do we diagnose diseases of the thyroid?

A

Diagnosis: based on TSH

A = high TSH + low T4 –> primary hypothyroidism

B = high T4 + low TSH –> primary hyperthyroidism

C = high TSH + high T4 –> TSH secreting pituitary adenoma (with a high T4, TSH should be low, so we know the TSH is being secreted autonomously)

D = low/normal TSH + low T4 –> central problem

Other: destructive thyroiditis due to infection that attacked the thyroid gland

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18
Q

Treatments of thyroid diseases?

A
  1. Medical therapy –> anti-thyroid medications (first hormones to normalize are T4 and T3, followed later on by TSH; process takes so long for the treatment to exert its effects fully because there is such a large reserve of thyroid hormone)
  2. Radioactive iodine
  3. Surgery
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19
Q

Central hypothyroidism is cause by what?

A

By impaired glycosylation, reduced bioactivity and prolonged serum half-life of TSH. It is therefore not converted and do not stimulate T4 and T3.

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20
Q

Where are cathecolamines and steroids produced?

A

In the addrenal gland: hybrid endocrine glands that produce 2 structurally distinct classes of hormones: Steroids (Adrenal Cortex) and Catecholamines (Adrenal Medulla)

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21
Q

Cathecolamine reaction production?

A

Tyrosine –> L-DOPA –> Dopamine –> Norepinephrine –> methyl group –> Adrenaline (epinephrine)

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22
Q

What is Pheochromocytoma?

A

An excess of cathecolamines:

  • Tumour of the adrenal gland that presents with symptoms such as episodes of palpitations, anxiety, headache, pallor and sweating.
  • Diagnosis: cathecolamines, metanephrines and MRI.
  • Treatment: alpha-blockers THEN beta-blockers (never beta-blocker BEFORE alpha-blockers!!) + normalization of blood pressure and high salt diet for volume expansion before surgery (tumour resection)
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23
Q

Steroid biosynthesis - 3 main pathways?

A
  1. Glomerulosa –> Mineralocorticoid –> Aldosterone
  2. Fasciculata –> Glucocorticoid –> Cortisol
  3. Reticularis –> Androgen –> Dehydroepiandrosterone (sex hormone precursor)
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24
Q

The common precursor of all steroid hormones is?

A

Cholesterol

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25
Q

Effect of ACTH?

A
  • Increase blood flow through the adrenal gland
  • Increase in steroid secretion
  • Trophic effects: increase in the size of the adrenal gland
  • So, important in both the size and function of the adrenal gland; No ACTH for many weeks = atrophic adrenal gland
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26
Q

Effect of cortisol?

A
  • Peaks in the morning
  • In the circulation, cortisol is largely bound to a glucocorticoid-binding protein (transcortin) and a fraction is bound to albumin; only 5% free. Therefore we only test FREE cortisol because it can be influence by pill or pregnancy.
  • Mechanism of regulation: CNS –> hypothalamus –> anterior pituitary –> adrenal cortex –> cortisol. Inhibitory feedback from cortisol levels in the plasma to the anterior pituitary gland
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27
Q

Cushing syndrome symptoms?

A
  • weight gain
  • fat pads
  • trunk obesity
  • proximal muscle weakness
  • baldness, moon-face
  • skin thinning
  • bruises
  • depression
  • insomnia
  • stops growth
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28
Q

Cushing syndrome diagnosis?

A
  1. Establishing the diagnosis

Valid screening tests of CS:

  1. 24 hour free cortisol: elevated
  2. Low dose Dexamethasone suppression test: Non suppressed
  3. Plasma cortisol measurements in the morning and in the evening (loss of circadian rhythm)
  4. Late-night salivary cortisol-elevated
  5. Establishing the cause
  6. ACTH-dependent ACTH HIGH
  7. CS-Pituitary ACTH
  8. Ectopic or adrenal tumour

Differentiated by high dose dexamethasone suppression test with cortisol in the morning

Treatment is laparoscopic adrenalectomy with corticoid prescription and low weaning

  1. Independent ACTH LOW (exogenous uses of glucocortidoids)
  2. Identify source of ACTH-dependent –> CIRCADIAN RYTHM
  3. Imaging
29
Q

Addison’s disease symptoms?

A
  • Pigmentation concentration
  • muscular weakness
  • loss of weight
30
Q

Addison’s disease diagnosis?

A
  1. Primary insufficiency (adrenal problem): ACTH levels are high + no response to ACTH
    * Treatment is cortisol and aldosterone for life
  2. Secondary (pituitary or hypothalamus problem): ACTH levels are low + weak response to ACTH + no rise of ACTH in response to insulin-induced hypoglycaemia
    * Just cortisol
31
Q

Primary Hyperaldosteronism

A
  • Low renin, high aldosterone
  • Clinical presentation: hypertension, hypokalemia
  • Differential: adrenal adenoma or adrenal hyperplasia
32
Q

Secondary Hyperaldosteronism

A
  • High renin, high aldosterone
  • econdary to chronically decreased arterial blood volume (heart failure, cirrhosis with ascites, nephrotic syndrome), renal artery stenosis, etc
33
Q

Endocrine Causes of Resistant Hypertension

A
  • Hyperaldosteronism (primary)
  • Cushing’s Syndrome
  • Pheochromocytoma
  • Hyperthyroidism
  • Acromegaly
34
Q

Type 1 diabetes?

A
  • No ß-cell, therefore no insulin
  • High glucagon
  • Have to inject insulin
35
Q

Type 2 diabetes?

A
  • Increased insulin resistance, decreased insulin secretion
  • Glucose levels very high but insulin levels don’t peak enough and don’t come back down (
  • Exercise, metformin and PPARy agonist are the treatment used
36
Q

How does insulin work?

A

Glucose sensors in the body: the pancreatic ß-cell (central part of the cells). These cells will secrete insulin, which will make the cells take up glucose, therefore decrease glucose concentration in blood. The glucose gets metabolized trough oxidation (ATP production) in pancreatic ß-cell the and the ATP binds to K+ channel and inactivates it. A drug inactivating a K+ channel would increase insulin secretion and potentially cause hypoglycemia. The K+ increases in the cells and the calcium influx is activated. The calcium influx in the cells will results in the fusion of the vesicles with insulin to the membrane and the release of it. The insulin will then travel to other cells in the body and make them metabolize glucose.

37
Q

Non-glucose regulators of insulin secretion at the ß-cell?

A
  • Incretins: in response to gut nutrients ® Gastric inhibitory peptide (GIP) and Glucagon like peptide-1 (GLP-1; used to treat type 2 diabetes, g-coupled-protein receptor)
  • Amino Acids: minor effect, most potently as combinations; best is leucine and glutamate
  • Fatty acids: activate fatty acid receptor, metabolized to long chain fatty acyl CoA and diacylglycerol which can stimulate insulin release, chronic stimulation by fatty acids leads to decreased insulin secretion
  • Estrogens stimulate insulin release
  • Leptin, melatonin, IGF-1 inhibit insulin release
38
Q

How does glucagon work?

A

Pancreatic a-cells will secrete glucagon, which will increase glucose levels in blood.

Liver

  • Stimulates glycogenolysis
  • Stimulates gluconeogenesis
  • Stimulates fatty acid oxidation to ketones

Adipose Tissue

  • Stimulates lipolysis

Insulin is the main factor that regulates the glucagon release. Other regulators include amino acids, GIP, CCK, adrenergic innervation, stress hormones, exercice, somatostatin, GLO-1 and leptin

39
Q

How does Metformin work?

A
  • Usually first line medication due to lack of hypoglycemia when used alone
  • No weight gain, possible weight loss
  • Decreased cardiovascular events (UKPDS study)
  • Excreted by kidney (cannot be used in renal failure)
  • Contraindicated in conditions that have high risk of lactic acidosis (renal failure, severe heart failure, liver insufficiency etc.)
  • GI upset occurs
40
Q

Insulins – Types and pharmacokinetics?

A
  • Short acting (regular insulin) – duration ~ 6 hours, peak 2-4 hours
  • Rapid acting (lispro, aspart, glulisine) - duration ~ 4 hours, peak 1-2 hours
  • Intermediate acting (NPH – neutral protamine Hagedorn) – duration ~18 hours, peak 8-12 hours
  • Long acting (detemir, glargine) – duration ~24 hours, minimal peaking
  • Very long acting (degludec) – duration ~40 hours, no peak
41
Q

When do we do a work up for a thyroid mass?

A
  • ≥1.5cm warrant workup (95% of thyroid nodules are benign)
  • Some <1.5cm warrant workup

*Exceptions: family history, big radiation history, and a smaller mass that really looks like cancer

42
Q

What is the Work-up of thyroid nodules?

A
  • Ultrasounds
  • Ultrasound guided biopsy
  • Molecular testing? the futur! BRAF is bery bad and we give radioactive ionide
43
Q

Treatment of thyroid cancer?

A
  • Surgery (a lot of nerve, very important)
  • +/- Radioactive iodine
  • Rarely external beam radiation and chemotherapy
44
Q

Most common type of thyroid cancer?

A
  1. Papillary carcinoma: psammoma bodies and nitranuclear vacuoles on histology, good prognosis, >70% of papillary thyroid cancers have point mutations of the BRAF and RAS genes, and RET/PTC rearrangements
  2. Follicular carcinoma: extracapsular spread and angioinvasion, good prognosis
  3. Medullary carcinoma: associated with mutations and MEN syndrome
45
Q

Graves’ disease

A
  • TSH
  • Medical management (usually) or surgery for the eyes
  • Risk of injuring the recurrent laryngeal nerve
46
Q

Hyperparathyroidism differentals?

A
  • Primary hyperparathyroidism: adenoma or hyperplasia (MOST COMMON)
  • Malignancy: PTH +++ and palpable
  • Familial Hypocalciuric Hypercalcemia
  • Other: Paget’s, Addisons, Sarcoidosis, Oral intake…
47
Q

History of someone presenting with hyperparathyroidism?

A
  • Kidney stones
  • Osteopeosis
  • Bone pain
  • Confusion
  • Fatigue
  • GI issues
48
Q

How do we diagnose hyperparathyroidism?

A
  1. Labs: serum calcium, PTH and 24 hour urine calcium
  2. Imaging:
  3. Nuclear Scan (parathyroid scan)
  4. Ultrasound if suspected parathyroid mass
  5. Dual energy CT scan
49
Q

Treatment of hyperparathyroidism?

A

1st Line: Methimazole / PTU and Metoprolol (beta-blocker for palpitations)

2nd Line: Radioactive iodine (small dose)

3rd Line: Surgery (sometimes 2nd line for the eyes)

50
Q

Types of Multiple Endocrine Neoplasia?

A
  • MEN I (Werner’s syndrome, hyperparathyroidism)
  1. Parathyroid hyperplasia
  2. Pancreatic tumors
  3. Pituitary adenomas
  • MEN IIa (Sipple syndrome, hyperparathyroidism, Medullary carcinoma​)
  1. Parathyroid hyperplasia
  2. Pheocromocytoma
  3. Medullary thyroid cancer
  • MEN IIb (NOT a type of hyperparathyroidism, Medullary carcinoma)
  1. Pheocromocytoma
  2. Medullary thyroid cancer
  3. Mucosal neuromas
  4. Marfanoid habitus
51
Q

Factors influencing growth?

A
  • Maternal malnutrition
  • Smoking, alcohol
  • AIDS, chronic illness, maternal infections
  • Nutritional intake
  • Repeated infections
  • Psychological stress
  • Sleep (GH peaks at night)
52
Q

Important hormones in normal growth?

A

Primary importance:

  • GH (GSH + / Somatostatin -): lipolysis, glycolysis (higher blood sugar) and chondrogenesis
  • Insulin-like growth factor (IGF) I and II (GH +, produced by the liver): chondrogenesis, protein synthesis and cell proliferation (a bit the contrary)
  • Adequate nutrition

Permissive effect:

  • Sex hormones (androgens and estrogens)
  • Thyroid hormones
  • Glucocorticoids
  • Insulin
53
Q

Abnormal growth diagnosis?

A
  • GH deficiency: test by stimulation test (exercise, hypoglycemia, arginine).
  • Constitutional delay: familial disorder, no treatment required
  • GH receptor mutation: Laron dwarfism (rare)
  • GH hypersecretion: gigantism if onset prior to puberty, acromegaly if adult onset, test by suppression test (oral glucose) and treated by surgery of medication
  • TH deficiency (intrauterine growth ++)
  • Testosterone deficiency
54
Q

3 different ages?

A
  1. Chronological age
  2. Height age
  3. Bone age
55
Q

Metabolism can be broken down into 2 big functions?

A
  1. Catabolism (energy-yielding nutriments –> chemical energy production –> energy-poor end products)
  2. Stage 1: hydrolysis of complex molecules to their component building blocks
  3. Stage 2: conversion of buildings blocks to acetyl CoA
  4. Stage 3: oxidation of acetyl CoA; oxidative phosphorylation
  5. Anabolism (precursor molecules –> use of chemical energy –> complex molecules)
56
Q

Glycolysis BIG equation?

A

2 ATP + 1 Glucose <–> 4 ATP + 2 NADH + 2 Pyruvate

57
Q

3 important enzymes moderated by insulin?

A
  1. Hexokinase: in tissues other than liver and pancreas, moderate maximal speed means tissues don’t take more glucose than they can use
  2. Glucokinase: in liver and pancreas, used by liver to soak up sugar from a meal (high maximal speed) and used by pancreas to sense glucose levels and control (insulin release), DRUG TARGET type 2 diabetes
  3. Phosphofructokinase I: transcription in the liver regulated by insulin (+) and glucagon (-)
58
Q

Why is the high sugar western diet leads to obesity?

A

Fructose bypasses regulation of glycolysis by GK FASTER GLYCOLYSIS

59
Q

Glycolysis errors and pathologies

A
  • In diabetes, glucose AND FAT homeostasis is de-regulated leading to hyperglycemia (hence the name) and a very large number of serious health risks
  • PDH deficiencies (enzyme that converts pyruvate to Acetyl-CoA): seen in children, elevated lactate and pyruvate in the blood (chronic lactic acidosis), severe neurological defects, usually lethal EX. Leight syndrome (French Canadian type)
  • Thiamine deficiency: thiamine is a vitamin required as a cofactor in PDH, alcoholics have deficiencies in making thiamine because decreased uptake and processing, leads to lactic acidosis EX. Wernicke-Korsakoff syndrome
  • Cyanide poisoning: stops ETC dead by CN- binding Fe3+ in complex IV, rapid cell death, CNS damage
  • Carbon monoxide poisoning: stops ETC by CO binding Fe2+ in complex IV
  • McArdle Disease: no phosphorylase in muscle, can’t do strenuous exercise, damage from inadequate energy supply and glycogen accumulation
  • Von Gierke Disease: no G-6-phosphatase in liver, fasting hypoglycemia and other metabolic consequences, treat by continuous supply of carbs, including via nasogastric tube while sleeping
60
Q

TCA cycle

A
  • Where the oxidative metabolism of carbohydrates, fats and amino acids converge
  • Occurs totally in the mitochondria
  • An AEROBIC pathway because it makes NADH and the cell need O2 to use the NADH to make ATP
  • Features in synthetic/anabolic pathways:
    1. Gluconeogenesis
    2. Amino acid synthesis
    3. Heme synthesis
  • NOT a closed isolated pathway, more like a roundabout
  • 2 carbons enter and they get burned, that is why we exhale CO2
  • We are stripping of electrons from an energetic molecules and pass them on to another one, it is an energy favorable process because is passes electrons to molecules that have higher affinity. The final receiver is oxygen, which is the molecule that has the most affinity with the electrons.
  • We pump H+ as we pass electrons
61
Q

Process of glucose synthesis by the liver?

A
  • Gluco-phosphatase is present in the LIVER (not in the muscles) and converts glucose-6-P into glucose to store it
  • Glygogen phosphorylase is also present in the LIVER to LYSE the glycogen chain (stimulated by glucagon) to increase blood sugar.
  • The liver feeds the other tissues by 2 ways:
  1. Mobilizing glucose stored as glycogen (glycogenolysis)
  2. Making new glucose (gluconeogenesis): uses 4 steps to get around the 3 irreversible reactions of glycolysis, to go from lactate to glucose stimulated by glucagon and acetyl-CoA
62
Q

The pyruvate is then converted into?

A
  1. Acetyl-CoA (normal response, TCA cycle)
  2. Ethanol (pathologic)
  3. Lactate (solid tumours = Warburg effect or low oxygen = lactic acidosis)
  4. Oxaloacetate
63
Q

Fatty synthesis is important for what?

A
  • Energy
  • Structure (cell membranes) MOST IMPORTANT
  • Function
  • Insulation
  • Padding
64
Q

Which 2 enzymes convert Acetyl Co-A into fatty acids?

A
  1. Acetyl-Co carboxylase (ACC): stimulated by insulin and citrate; inhibited by glucagon, adrenaline, AMP and palmotoyl-CoA. It can also be a pharmalogical target to reduce weight.
  2. Fatty acid synthase: will form the palmitase, also a possible drug target
65
Q

We store fatty acid into adipose tissue or we add it/derivative it to complex fatty acids by other pathway requiring enzymes such as?

A
  1. Phospholipids for cell membrane
  2. Sphingomyelin in grey manner and nerves
  3. Ganglioside GM2: electrical transmission
66
Q

Metabolic disease – deficiency in fatty acids synthesis ?

A
  • Niemann-Pick disease: spingomyelinade deficiency, death in early childhood
  • Gancher disease: accumulation of gluco-cerebrosides
  • Tay-sachs disease: accumulation of gangliosides, neurodegeneration
  • GM1 gangliosidosis: accumulation of gangliosides and keratin sulphate
67
Q

What important enzymes plays a role in β-Oxidation of fatty acids?

A

Acyl-CoA Dehydrogenase

Common deficiency that causes accumulation of fatty acids

68
Q

What is the role of carnitine in the fatty acid mobilization?

A

Carnitine transports the fatty acid in the mitochondria where it can be transformed into energy. Carnitine deficiency leads to decreased ability to use Long chain Fatty acids, toxic accumulation of FA and hypoglycemia (liver needs ATP to make glucose). Ketosis will occur if you are in extreme starvation.

69
Q

What can a lack of insulin induce?

A

Bloc E - Digestion and metabolism (6 decks)

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