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Pathophysiology > week 6 > Flashcards

week 6 Flashcards

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1
Q

endocrine control

A

endocrine system is a complex network of cells and glands that produce and release hormones, which are chemical messengers that travel through the bloodstream to regulate various physiological activities in the body

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2
Q

what controls the endocrine system

A

Hypothalamus

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3
Q

The anterior pituitary releases:

A

Thyroid-stimulating hormone (TSH)
Adrenocorticotropic hormone (ACTH)
Growth hormone (GH)
Prolactin (PRL)
Gonadotropins (LH and FSH)

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4
Q

the hypothalamus produces hormones called

A

Thyrotropin-releasing hormone (TRH)
Corticotropin-releasing hormone (CRH)
Growth hormone-releasing hormone (GHRH)
Prolactin-releasing hormone (PRH)
Gonadotropin-releasing hormone (GnRH)

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5
Q

thyroid produces

A

T3 (triiodothyronine)
T4 (thyroxine)

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6
Q

parathyroid hormone, action

A

increases blood calcium levels, opposing calcitonin from the thyroid

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7
Q

Thymus Gland: role

A

production and maturation of immune cells including small lymphocytes that protect the body against foreign antigens.

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8
Q

Adrenal Glands release consist of a cortex and medulla

A

cortex releases cortisol and aldosterone, which help regulate metabolism and blood pressure
medulla produces adrenaline and noradrenaline, involved in the fight-or-flight response

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9
Q

Pancreas releases

A

insulin and glucagon to regulate blood glucose levels (opposing hormones)

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10
Q

kidneys release

A

renin, increases blood pressure, and erythropoietin, which stimulates red blood cell production

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11
Q

Mechanisms of Endocrine Hypofunction

A

Ageing: Hormone production can decline with age, affecting various endocrine glands
Autoimmune Conditions: certain autoimmune diseases can attack hormone-secreting cells, leading to reduced hormone levels
Infections and Inflammation: these can damage endocrine tissues, impairing hormone production
Drug Effects: Some medications can cause atrophy of hormone-producing cells, further reducing hormone levels

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12
Q

Causes of Endocrine Hyperfunction

A

Hyperplasia or Hypertrophy
Tumours
Autoimmune Disorder

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13
Q

hypothalamus role

A

maintaining homeostasis by regulating endocrine, autonomic, behavioral, and circadian functions

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14
Q

Anterior Nucleus (Preoptic area) function, impairment and mechanism

A

Function: Mediates heat dissipation via parasympathetic activation (e.g., vasodilation, sweating)
Impairment: Leads to hyperthermia or poor thermoregulation, especially in febrile states
Mechanism: Impaired central inhibition of heat-retention pathways

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15
Q

Posterior Nucleus function, impairment and mechanism

A

Function: Promotes heat conservation via sympathetic activation (e.g., vasoconstriction, shivering)
Impairment: Results in hypothermia and inability to respond to cold exposure
Mechanism: Disruption of descending sympathetic outflow from the hypothalamus

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16
Q

Ventromedial Nucleus (VMH) function, impairment and mechanism

A

Function: Satiety center; inhibits feeding behaviour
Impairment: Leads to hyperphagia and obesity—seen in lesions like craniopharyngioma
Mechanism: Leptin receptor–mediated appetite control is disrupted

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17
Q

Lateral Nucleus: function, impairment and mechanism

A

Function: Stimulates hunger and feeding behaviour
Impairment: Causes anorexia, weight loss, and failure to thrive, especially in paediatric populations
Mechanism: Disruption in orexin and melanin-concentrating hormone signaling pathways

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18
Q

Supraoptic Nucleus: Arcuate Nucleus: function, impairment and mechanism

A

Function: Key regulator of the tuberoinfundibular pathway, modulating dopamine (inhibitory to prolactin), GnRH, GHRH, and appetite-related peptides
Impairment: May result in hyperprolactinaemia, amenorrhea, growth delay and appetite dysregulation
Mechanism: Dysfunction of neuropeptide signaling and hypothalamic-pituitary communication

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19
Q

Paraventricular Nucleus (PVN): function, impairment and mechanism

A

Function: Produces oxytocin and CRH, and regulates autonomic output
Impairment: Causes decreased oxytocin (impacting parturition, lactation, and bonding) and dysregulated stress response via altered CRH secretion
Mechanism: Neuroendocrine axis impairment, particularly the HPA axis

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20
Q

Suprachiasmatic Nucleus (SCN): function, impairment and mechanism

A

Function: Acts as the central circadian pacemaker, synchronizing biological rhythms via light cues from the retina
Impairment: Leads to circadian rhythm disorders, such as sleep phase delay, insomnia, or irregular sleep-wake cycles
Mechanism: Disruption in melatonin regulation and clock gene expression

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21
Q

Supraoptic Nucleus: function, impairment and mechanism

A

Function: Produces vasopressin (ADH) for water balance
Impairment: Leads to central diabetes insipidus with polyuria, polydipsia, and hypernatraemia
Mechanism: Loss of AVP synthesis and axonal transport to the posterior pituitary

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22
Q

Aetiology of Hypothalamus dysfunction

A

Intracranial masses
Vascular events
Trauma or surgery:
Medications
Inflammatory and infectious processes

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23
Q

hypothalamic peptides directly affect

A

functions of the thyroid gland, the adrenal gland, and the gonads as well as influencing growth, milk production and water balance

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24
Q

infundibulum connects what

A

hypothalamus and pituitary gland

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25
how does the hypothalamus comunicate with the Anterior Pituitary Gland
through a blood supply
26
how does the hypothalamus comunicate with the posterior Pituitary Gland
via nerve signals, allowing for direct hormonal release without the need for blood transport
27
Hypopituitarism
efers to decreased secretion of pituitary hormones, which can result from either disease of pituitary gland or hypothalamus
28
Aetiology of hypopituitarism
Pituitary Disorders: impair secretion of one or more hormones commonly due to mass lesions, infarction or iatrogenic e.g., from pituitary adenoma surgery, radiation)
29
Clinical manifestations of hypopituitarism
Patients may be asymptomatic or present with symptoms related to hormone deficiency
30
where is the growth hormone produced in what cell
pituitary somatotroph cells
31
growth hormone role
growth and metabolism
32
* Hyperfunction: excessive hormone production of endocrine function causes
* Excessive stimulation and hyperplasia or hypertrophy of the endocrine gland * Hormone-producing tumour of the gland * Ectopic hormone secretion * Medication * Decrease negative feedback
33
anterior pituitary hormones impoertant ones to know secreted here are
growth hormone thyroid hormone and Adrenocortictropic
34
Causes of multi-hormone pituitary disruptions
* Tumours * Pituitary surgery or radiation * Lesions and head trauma * Infection or inflammation * Autoimmune disease
35
Clinical manifestations of hypopituitarism
* Headache * Altered mental state * Postural hypotension * Being chronically unfit * Weakness and fatigue * Growth failure
36
Growth hormone excess and deplition excretion
* Excess – gigantism (children), acromegaly (adults) * Depletion – dwarfism (children)
37
ADH excess and deplition excretion
* Excess – SIAHD * Depletion – Diabetes insipidus
38
ACTH excess and deplition excretion
* Excess – Cushing’s * Depletion – Addison’s
39
Growth hormone hyposecretion - children
delayed puberty * Delayed skeletal maturation * Results in short stature or dwarfism * Disrupts normal blood glucose levels * Decreased muscle mass * Increased subcutaneous fat
40
Growth hormone hyposecretion - adult
* Reduced bone density * Alterations in physical and mental well-being * Cardiac function and metabolic parameters * Lower levels of energy and libido
41
Growth hormone hypersecretion - children
* Results in increased linear bone growth – Gigantism * Thickening of fingers, jaw, forehead, hands and feet * Decreased bone density
42
Growth hormone hypersecretion - adults
* Overgrowth of the cartilaginous parts of the skeleton * Enlargement of the heart and other organs of the body * Metabolic disturbances resulting in altered fat metabolism and impaired glucose tolerance
43
main function of adrenal gland
Stress responsiveness Sugar (glucose) availability Salt balance Sexual balance and maintenance
44
Adrenal Medulla
part of the sympathetic nervous system when stimulated releases adrenaline and noradrenaline
45
Primary Adrenal Insufficiency (Addison’s Disease)
adrenal cortex (outer layer of adrenal gland). Leads to ↓ cortisol, ↓ aldosterone, and ↓ adrenal androgens
46
Aetiology Primary Adrenal Insufficiency
Autoimmune adrenalitis (most common) - autoimmune process that destroys the adrenal cortex;
47
Epidemiology Primary Adrenal Insufficiency
2500 australians with 100 new dx each year
48
B. Seconday Adrenal Insufficiency is problem in
pituitary gland (↓ACTH). Aldosterone is preserved.
49
C. Tertiary Adrenal Insufficiency is problem in the
hypothalamus (↓CRH) or functional suppression of Hypothalamic-Pituitary-Adrenal axis
50
aeitology of Tertiary Adrenal Insufficiency
Most common - Exogenous glucocorticoids Long-term steroid therapy (oral, inhaled, topical, intra-articular) Abrupt cessation of steroids without tapering Hypothalamic tumours or trauma
51
Clinical manifestations of Primary Adrenal Insufficiency (Addison’s Disease)
fatigue, weakness, nausea, anorexia and weight loss, abdominal pain, darkening of the skin or mucous membranes chronic hypotension, hypoglycaemia, decreased heart size
52
Zona glomerulosa (outer) adrenal cortex, hormone produced and its function
Mineralocorticoids (mainly aldosterone) Regulates sodium and potassium balance via the RAAS
53
Zona fasciculata (middle) adrenal cortex, hormone produced and its function
Glucocorticoids (mainly cortisol) Controls metabolism, immune response, and stress response. Secretion is regulated by the hypothalamic-pituitary-adrenal axis via ACTH
54
Zona reticularis (inner) adrenal cortex, hormone produced and its function
Androgens (e.g., DHEA) Contributes to secondary sexual characteristics, especially in females
55
Negative feedback in Adrenal Medulla
High cortisol inhibits both CRH and ACTH production
56
Subclinical/Partial adrenal cortex
Mild or absent symptoms; often normal cortisol at rest but inadequate during stress
57
Compensated/Chronic adrenal cortex clinical manifestations
Progressive fatigue, anorexia, weight loss, postural hypotension, hyperpigmentation
58
Acute Adrenal Crisis
life-threatening hypotension, shock, vomiting, abdominal pain, hypoglycaemia
59
Cushing Syndrome
characterised by elevated cortisol levels in the blood, which can arise from various causes, including both exogenous and endogenous factors
60
Exogenous Cushing Syndrome Aetiology
cortisol is introduced from outside the body, commonly through long-term use of steroid medication
61
Endogenous Cushing Syndrome
results from the body producing excess cortisol.
62
Pathogenesis Cushing Syndrome
involves the dysregulation of the hypothalamic-pituitary-adrenal axis. Normally, the hypothalamus releases corticotropin-releasing hormone, stimulating the pituitary gland to secrete ACTH, which in turn prompts the adrenal glands to produce cortisol In Cushing syndrome, this regulatory mechanism is disrupted, leading to abnormally high cortisol levels
63
clinical manifestations of Cushing syndrome
Muscle Wasting Skin Changes Bone Health
64
Addison’s Disease is compared to ushing Syndrome
Addison’s Disease (Primary Adrenal Insufficiency) Cushing Syndrome (Glucocorticoid Excess)
65
Addison’s Disease (Primary Adrenal Insufficiency) cause, hormonal deficientcies and clinical features
Cause: Autoimmune destruction of the adrenal cortex (autoimmune adrenalitis), infections (e.g., TB, CMV), hemorrhage, infiltrative disease, or medications Hormones Deficient: ↓ Cortisol, ↓ Aldosterone, ↓ Androgens Clinical Features: fatigue, weight loss, nausea, vomiting, postural hypotension, hyperpigmentation
66
Cushing Syndrome (Glucocorticoid Excess) cause, hormonal deficientcies and clinical features
Cause: Prolonged exposure to excess cortisol Exogenous steroids (most common) Endogenous: Pituitary adenoma (Cushing disease), adrenal tumor, ectopic ACTH Hormones Elevated: ↑ Cortisol (± ACTH depending on source) Clinical Features: central obesity, moon face, buffalo hump, muscle wasting, skin thinning, purple striaem hypertension, glucose intolerance, osteoporosis
67
Thyroid gland secrete what 3 hormones
Thyroxine (T4) Triiodothyronine (T3) Calcitonin
68
Thyroid disorders Epidemiology
not readily known
69
Hypothyroidism Aetiology
Primary hypothyroidism is due to inadequate production of thyroid hormone caused by disease of the thyroid gland
70
Hyperthyroidism Aetiology
Increased thyoid hormone synthesis: Exogenous thyroid hormone use Increased release of preformed throid hormone:
71
Thyroid storm
rare but severe presentation of hyperthyroidism characterised by an acute exacerbation of symptoms
72
clinical manifestations of thyroid storm
Anxiety and irritability Sweating and heat intolerance Tachycardia Weight Loss Fatigue
73
Describe the role of thyroid hormones in metabolism
Increase Basal Metabolic Rate Carbohydrate Metabolism Lipid Metabolism Protein Metabolism
74
Clinical presentations of hypothyroidism include:
Weight Gain Fatigueadequate rest Dry Skin and Hair Loss Constipation
75
Hyperthyroidism Clinical features include
Weight Loss Anxiety and Irritability Tachycardia Frequent Loose Stools
76
parathyroid glands secrete what hormone and what is its function
parathyroid hormone (PTH) which is a major regulator of calcium balance
77
Hypoparathyroidism Aetiology
Post-surgical autoimmune destruction Genetic causes Infiltrative diseases
78
Hypoparathyroidism Pathophysiology
deficient secretion or action of parathyroid hormone (PTH). reduced calcium reabsorption in kidneys and bones There is also low or inappropriately normal active form of Vitamin D levels, and this leads to less intestinal calcium absorption
79
Clinical manifestations Hypoparathyroidism
Neuromuscular irritability e.g., muscle cramps, facial twitching, paraesthesias Psychiatric symptoms Chronic: dry skin, brittle nails, hair loss, basa
80
Primary Hyperparathyroidism Aetiology
Autonomous overproduction of PTH, typically due to: Parathyroid adenoma (most common) Hyperplasia Rarely, parathyroid carcinoma
81
Primary Hyperparathyroidism pathophysiology
Hypercalcaemia via increased bone resorption, increased calcium reabsorption from kidneys, and increased intestinal absorption as there is an increase conversion of Vitamin D to its active form
82
Secondary Hyperparathyroidism Aetiology and Pathophysiology
Chronic kidney disease (CKD) → impaired vitamin D activation and phosphate retention Vitamin D deficiency or malabsorption
83
Clinical manifestations of Hyperparathyroidism
Skeletal: Osteopenia/osteoporosis Renal: Nephrolithiasis (calcium stones) Gastrointestinal: Constipation, nausea Neuromuscular: Fatigue, weakness Psychiatric: Depression Cardiac: Shortened QT interval, arrhythmia
84
Diabetes Mellitus
condition marked by high levels of glucose (sugar) in the blood.
85
Type 1 diabetes
* Characterised by extensive damage to the pancreatic beta islet cells * Insulin production and release is reduced
86
Development of Type 1A Diabetes
* Genetic predisposition * Immunologically mediated beta cell destruction
87
Idiopathic Type 1B Diabetes
* Those cases of beta cell destruction in which no evidence of autoimmunity is present * Strongly inherited.
88
Aetiology of T1DM
1. Autoimmune Origin- caused by immune-mediated destruction of pancreatic β-cells 2. Genetic Susceptibility 3. Environmental Triggers- Viruses, Diet, Toxins, Immunotherapy
89
Epidemiology of T1DM
most common chronic diseases in childhood Approximately 13,200 children and young adults aged 0–19 were living with type 1 diabetes in 2021 first nations children= a lot more common
90
Pathogenesis of T1DM
a lack of endogenous insulin secretion from the pancreatic β-cells
91
stages of T1DM
Autoimmunity Begins Early Glucose Changes Clinical Diabetes
92
Clinical manifestations of T1DM
increased urinary glucose excretion enhanced thirst Weight loss Acute visual disturbances
93
Complications of T1DM
developing eye damage developing nervous system damage developing kidney disease being diagnosed with a second autoimmune disease
94
Type 2 Diabetes Mellitus
characterised by hyperglycaemia, insulin resistance and defective insulin secretion
95
Type 2 Diabetes Mellitus Aetiology
1. Genetic Predisposition 2. Lifestyle and Environmental Factors
96
T2DM Epidemiology
In Australia, there are over 1.2 million (4.6%) people were living with type 2 diabetes
97
T2DM Pathophysiology
multifactorial- may have: insulin resistance in muscle, adipose tissue, and liver defective insulin secretion
98
Impaired insulin processing in T2DM
a greater proportion of secreted insulin remains as proinsulin This suggests that the processing of proinsulin to insulin in the β-cells is impaired in T2DM
99
Clinical manifestations of T2DM
increased urinary glucose excretion, blurred vision, fatigue or feeling tired and weight loss
100
Definition Metabolic syndrome
cluster of common abnormalities, including insulin resistance, impaired glucose tolerance, abdominal obesity, reduced high-density lipoprotein (HDL)-cholesterol levels, elevated triglycerides, and hypertension.
101
Diagnostic Criteria (≥3 of 5 components) of Metabolic syndrome (MetS)
abdominal obesity elevated triglycerides: ≥150 mg/dL reduced HDL-C elevated blood pressure hyperglycaemia
102
Aetiology Metabolic syndrome
Visceral adiposity and ectopic fat accumulation Adipose tissue dysfunction Genetic susceptibility Sex-based hormonal differences Socio-environmental drivers
103
Pathogenesis of metabolic syndromes
At the core of these processes are visceral fat accumulation, insulin resistance and chronic low-grade inflammation which together lead to widespread metabolic and organ dysfunction.
104
Clinical manifestations of metabolic syndrome
obesity-related conditions hypertension-related signs: insulin resistance signs: fatigue dyslipidaemia
105
Overweight and Obesity Aetiology
Biological and Genetic Factors- Heritability& hormonal response to weight loss Behavioral and Environmental Factors: High caloric intake, ultra-processed foods, sedentary lifestyles and reduced sleep contribute significantly Developmental Origins- Foetal overnutrition, maternal obesity and early-life exposures can induce long-lasting changes in metabolism Iatrogenic Factors- certain meds
106
Phases of metabolism
Anabolism Catabolism Metabolites
107
Health risk for obesity
* Gallbladder disease, infertility * Sleep apnoea and pulmonary dysfunction * Cancer * Bone and joint problems Hypertension
108
Epidemiology of obesity
Adults: 66% children and Adolescents (2–17 years): 26%
109
Pathogenesis Overweight and Obesity
body defends its equilibrium fat stores triggered by reduced leptin and gut hormones that increase hunger and lower energy expenditure
110
Metabolic Consequences of obesity
This raises the workload on pancreatic β-cells
111
Cardiovascular Effects of obesity
Link between obesity and CVD is complex due to overlapping risk factor
112
Upper airways and respiratory system due to obesity
Physical effects of increased intra-abdominal and central adiposity on diaphragmatic compliance and lung function can also contribute to breathlessness
113
Musculoskeletal due to obesity
Weight-related metabolic and inflammatory factors contribute to direct mechanical

Pathophysiology (14 decks)

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