1
Q
What is endocrinology?
A
The study of hormones, the glands that release them, and the target organs they act upon.
2
Q
What is homeostasis?
A
Maintenance of a stable internal environment despite external or internal changes.
3
Q
How does the endocrine system help maintain homeostasis?
A
By releasing hormones that coordinate and regulate cellular and organ function across the body.
4
Q
What is a hormone?
A
A chemical messenger secreted by living cells in small amounts that travels, usually via the bloodstream, to distant targets where it regulates cellular activity.
5
Q
What are the major roles of hormones in the body?
A
Regulation of internal environment, metabolism, growth and development, and reproduction.
6
Q
How do hormones regulate the internal environment?
A
By controlling variables such as water balance, ion concentrations, cardiovascular function, and metabolic activity.
7
Q
What are endocrine glands?
A
Organs specialized to synthesize and secrete hormones directly into the bloodstream.
8
Q
Why are hormones suited for long‑term regulation?
A
Because they circulate in the bloodstream and can produce sustained systemic effects.
9
Q
What is negative feedback in endocrine systems?
A
A regulatory mechanism in which the final hormone or physiological effect inhibits earlier steps in the pathway.
10
Q
What is positive feedback in endocrine systems?
A
A mechanism where the final hormone enhances further hormone release, amplifying the response.
11
Q
What is a hormonal axis?
A
A multi‑level regulatory pathway involving the hypothalamus, pituitary gland, and peripheral endocrine organs.
12
Q
What are the three main levels of many endocrine axes?
A
Hypothalamus (master regulator), pituitary gland (regulator), and peripheral endocrine organ.
13
Q
What is the role of the hypothalamus in endocrine control?
A
It integrates neural signals and secretes releasing hormones that control pituitary hormone secretion.
14
Q
What is the role of the pituitary gland?
A
It releases tropic hormones that regulate the activity of peripheral endocrine glands.
15
Q
What are tropic hormones?
A
Hormones that act on other endocrine glands to stimulate hormone production and secretion.
16
Q
What are examples of classical endocrine glands?
A
Pituitary gland, thyroid gland, adrenal glands, pancreas, and gonads.
17
Q
Which non‑classical tissues can also secrete hormones?
A
Heart, liver, kidney, adipose tissue, GI tract, placenta, and hypothalamus.
18
Q
What is autocrine signalling?
A
A form of cell signalling where a cell releases a hormone that acts on itself.
19
Q
What is paracrine signalling?
A
A signalling mechanism where a hormone acts locally on nearby cells.
20
Q
What are the main classes of hormones?
A
Peptide/protein hormones, steroid hormones, and amine (tyrosine‑derived) hormones.
21
Q
How are peptide hormones synthesized?
A
They are produced as pre‑prohormones in the rough endoplasmic reticulum and processed into active hormones.
22
Q
Where are peptide hormones stored before release?
A
In secretory vesicles within endocrine cells.
23
Q
How are peptide hormones released?
A
By exocytosis in response to cellular stimulation.
24
Q
How are steroid hormones synthesized?
A
From cholesterol through enzymatic reactions mainly in mitochondria and smooth ER.
25
Are steroid hormones stored in vesicles?
No, they are synthesized on demand and diffuse out of cells.
26
What amino acid is the precursor for many amine hormones?
Tyrosine.
27
Which hormones are examples of tyrosine‑derived hormones?
Thyroid hormones, catecholamines (adrenaline and noradrenaline), and dopamine.
28
How are hormones transported in the blood?
Either dissolved in plasma or bound to transport proteins.
29
Which hormones usually circulate freely in plasma?
Peptide hormones and catecholamines.
30
Which hormones are mostly bound to transport proteins?
Steroid hormones and thyroid hormones.
31
Why do some hormones require transport proteins?
Because they are lipid‑soluble and poorly soluble in plasma.
32
What is the advantage of hormone‑binding proteins?
They prolong hormone half‑life and act as a circulating reservoir.
33
How do peptide hormones exert their effects?
By binding to cell‑surface receptors and activating intracellular signalling pathways.
34
Why can't peptide hormones cross the cell membrane easily?
Because they are water‑soluble and the membrane is lipid‑based.
35
What is a second messenger?
An intracellular signalling molecule that transmits signals from hormone receptors to cellular targets.
36
How do steroid hormones exert their effects?
By diffusing through cell membranes and binding intracellular receptors that regulate gene transcription.
37
Where are receptors for steroid hormones typically located?
In the cytoplasm or nucleus of target cells.
38
How do thyroid hormones exert their effects?
They enter cells and bind nuclear receptors that regulate gene expression.
39
What gland produces thyroid hormones?
The thyroid gland.
40
Where is the thyroid gland located?
In the neck, anterior to the trachea.
41
What are the two main thyroid hormones?
Thyroxine (T4) and triiodothyronine (T3).
42
Which thyroid hormone is more biologically active?
Triiodothyronine (T3).
43
What element is essential for thyroid hormone synthesis?
Iodine.
44
What is the first step in thyroid hormone synthesis?
Active uptake of iodide into thyroid follicular cells.
45
What protein transports iodide into thyroid cells?
The sodium‑iodide symporter.
46
What enzyme oxidizes iodide during thyroid hormone synthesis?
Thyroid peroxidase.
47
What protein serves as the scaffold for thyroid hormone synthesis?
Thyroglobulin.
48
What are MIT and DIT in thyroid hormone synthesis?
Monoiodotyrosine and diiodotyrosine, iodinated tyrosine residues on thyroglobulin.
49
How is T3 formed during synthesis?
By coupling one MIT with one DIT.
50
How is T4 formed during synthesis?
By coupling two DIT molecules.
51
How are thyroid hormones released from the thyroid gland?
Thyroglobulin is endocytosed, digested, and T3 and T4 are released into the bloodstream.
52
How are thyroid hormones transported in blood?
Mostly bound to plasma proteins such as thyroxine‑binding globulin.
53
What is the main function of thyroid hormones?
To regulate metabolism, growth, and development.
54
How do thyroid hormones affect metabolism?
They increase basal metabolic rate and oxygen consumption.
55
How do thyroid hormones affect the cardiovascular system?
They increase heart rate and cardiac output.
56
What hypothalamic hormone regulates the thyroid axis?
Thyrotropin‑releasing hormone (TRH).
57
What pituitary hormone stimulates the thyroid gland?
Thyroid‑stimulating hormone (TSH).
58
What is the hypothalamic‑pituitary‑thyroid (HPT) axis?
A regulatory pathway controlling thyroid hormone production through TRH, TSH, and thyroid hormones.
59
How do thyroid hormones regulate their own production?
Through negative feedback on the hypothalamus and pituitary.
60
What is hypothyroidism?
A condition characterized by insufficient thyroid hormone production.
61
What are common symptoms of hypothyroidism?
Fatigue, weight gain, cold intolerance, constipation, dry skin, and slowed thinking.
62
What physical sign may occur in hypothyroidism?
Goitre (enlargement of the thyroid gland).
63
What is the hypothalamo‑pituitary‑adrenal (HPA) axis?
A hormonal pathway that regulates the body's response to stress.
64
Which hypothalamic hormone starts the HPA axis?
Corticotropin‑releasing hormone (CRH).
65
Which pituitary hormone is released in response to CRH?
Adrenocorticotropic hormone (ACTH).
66
Which gland responds to ACTH?
The adrenal cortex.
67
What hormone is produced by the adrenal cortex in the stress response?
Cortisol.
68
What are the main actions of cortisol?
Increases glucose availability, suppresses immune responses, and helps the body respond to stress.
69
How does cortisol regulate its own production?
By negative feedback on the hypothalamus and pituitary.
70
Why is endocrine function assessed clinically?
To diagnose hormone excess or deficiency and evaluate endocrine gland function.
71
What are common methods of assessing endocrine function?
Measuring hormone levels in blood or urine and using stimulation or suppression tests.
72
Why are dynamic endocrine tests sometimes needed?
Because hormone secretion is often pulsatile and regulated by feedback loops.
73
What is a stimulation test?
A test that evaluates whether an endocrine gland can respond to a stimulating signal.
74
What is a suppression test?
A test that evaluates whether hormone secretion can be appropriately suppressed.
75
Why is understanding endocrine axes important in medicine?
Because many endocrine disorders result from dysfunction at different levels of the axis.
76
How do endocrine disorders affect homeostasis?
They disrupt normal regulation of physiological systems such as metabolism, fluid balance, and stress responses.
77
What is immunodeficiency?
A condition in which one or more components of the immune system are absent or function poorly, leading to increased susceptibility to infections.
78
What are the two main categories of immunodeficiency?
Primary immunodeficiency and secondary (acquired) immunodeficiency.
79
What is primary immunodeficiency?
Immunodeficiency caused by inherited genetic defects affecting components of the immune system.
80
What is secondary immunodeficiency?
Immunodeficiency resulting from external factors such as infections, malnutrition, drugs, or systemic disease.
81
What immune components may be affected in immunodeficiency?
B cells, T cells, combined B and T cells, phagocytes, or complement proteins.
82
How do B‑cell deficiencies typically present clinically?
Recurrent bacterial infections, particularly with encapsulated organisms.
83
How do T‑cell deficiencies typically present clinically?
Severe viral, fungal, and opportunistic infections.
84
What are combined immunodeficiencies?
Conditions where both T‑cell and B‑cell function are impaired.
85
What is Severe Combined Immunodeficiency (SCID)?
A group of genetic disorders characterized by profound defects in both T‑cell and B‑cell immunity.
86
What are phagocyte defects?
Disorders where neutrophils or macrophages cannot effectively kill pathogens.
87
What is Chronic Granulomatous Disease?
A phagocyte disorder caused by defective oxidative burst leading to impaired killing of pathogens.
88
What are complement deficiencies?
Conditions where complement proteins are absent or dysfunctional, impairing immune defense.
89
What types of infections are common in complement deficiencies?
Recurrent infections with encapsulated bacteria such as Neisseria species.
90
What are common causes of secondary immunodeficiency?
HIV infection, malnutrition, chemotherapy, immunosuppressive drugs, cancer, and chronic diseases.
91
How does HIV cause immunodeficiency?
By infecting and destroying CD4+ T helper cells, impairing immune coordination.
92
How can malnutrition cause immunodeficiency?
By impairing immune cell production and reducing immune responses.
93
How do immunosuppressive drugs cause immunodeficiency?
By suppressing immune cell activation or proliferation.
94
How does immunodeficiency affect immune responses?
It reduces the body's ability to recognize and eliminate pathogens effectively.
95
Why are patients with immunodeficiency prone to recurrent infections?
Because their immune system cannot mount effective responses to pathogens.
96
What is autoimmunity?
A condition in which the immune system mistakenly attacks the body's own tissues.
97
How can immunodeficiency lead to autoimmune disease?
Defective immune regulation may allow autoreactive immune cells to survive.
98
What is hypothyroidism?
A condition where the thyroid gland produces insufficient thyroid hormones.
99
How can immune dysfunction contribute to hypothyroidism?
Autoimmune attack on thyroid tissue can impair hormone production.
100
What autoimmune disease commonly causes hypothyroidism?
Hashimoto's thyroiditis.
101
What happens to the thyroid gland in Hashimoto's thyroiditis?
Immune cells infiltrate the gland and gradually destroy thyroid tissue.
102
What antibodies are commonly present in Hashimoto's thyroiditis?
Anti-thyroid peroxidase (TPO) and anti-thyroglobulin antibodies.
103
What are common symptoms of hypothyroidism?
Fatigue, weight gain, cold intolerance, dry skin, and slowed metabolism.
104
How can immunodeficiency alter susceptibility to autoimmune thyroid disease?
Immune dysregulation may increase risk of autoimmune responses against the thyroid.
105
What clinical features suggest immunodeficiency?
Recurrent infections, unusual infections, poor response to vaccines, and chronic inflammation.
106
How is immunodeficiency diagnosed?
Through clinical history, blood tests measuring immune cells, antibodies, and functional immune assays.
107
What is immunodeficiency?
Failure or reduced function of one or more components of the immune system leading to increased susceptibility to infection.
108
What are the two major categories of immunodeficiency?
Primary (genetic) immunodeficiency and secondary (acquired) immunodeficiency.
109
What is primary immunodeficiency?
Inherited genetic defects that impair the development or function of the immune system.
110
What is secondary immunodeficiency?
Acquired impairment of immune function caused by external factors such as infection, drugs, or malnutrition.
111
Which components of the immune system can be affected in immunodeficiency?
B cells, T cells, combined lymphocytes, phagocytes, or complement proteins.
112
What is the main clinical feature of immunodeficiency disorders?
Increased susceptibility to recurrent or severe infections.
113
What is the difference between innate and adaptive immune defects in immunodeficiency?
Innate defects affect early pathogen defence; adaptive defects affect antigen‑specific immune responses.
114
What characterizes B‑cell immunodeficiencies?
Reduced or absent antibody production.
115
What infections are typical in B‑cell immunodeficiency?
Recurrent bacterial infections, especially with encapsulated organisms.
116
Why are encapsulated bacteria common in antibody deficiency?
Antibodies are required for opsonisation and clearance of encapsulated pathogens.
117
What characterizes T‑cell immunodeficiencies?
Defective cell‑mediated immunity and impaired coordination of immune responses.
118
What infections are common in T‑cell deficiencies?
Viral, fungal, and opportunistic infections.
119
What are combined immunodeficiencies?
Disorders affecting both T‑cell and B‑cell immunity.
120
What is Severe Combined Immunodeficiency (SCID)?
A life‑threatening genetic disorder causing severe defects in both T‑cell and B‑cell function.
121
What infections occur in SCID?
Severe, recurrent bacterial, viral, fungal, and opportunistic infections.
122
What are phagocyte disorders?
Conditions where neutrophils or macrophages cannot effectively ingest or destroy pathogens.
123
What infections are common in phagocyte defects?
Recurrent bacterial and fungal infections, especially skin and organ abscesses.
124
What is Chronic Granulomatous Disease?
A disorder where phagocytes cannot produce reactive oxygen species to kill microbes.
125
What are complement deficiencies?
Defects in complement proteins involved in pathogen destruction and inflammation.
126
What infections are common in complement deficiencies?
Recurrent infections with encapsulated bacteria, particularly Neisseria species.
127
What are common causes of secondary immunodeficiency?
HIV infection, malnutrition, cancer, chemotherapy, immunosuppressive drugs, and chronic disease.
128
How does HIV cause immunodeficiency?
By infecting and destroying CD4+ T helper cells.
129
Why are CD4+ T cells important in immunity?
They coordinate immune responses by activating B cells, cytotoxic T cells, and macrophages.
130
How does malnutrition impair immunity?
It reduces immune cell production and weakens immune responses.
131
How do immunosuppressive drugs cause immunodeficiency?
They inhibit immune cell activation or proliferation.
132
Why can chemotherapy cause immunodeficiency?
It suppresses bone marrow, reducing white blood cell production.
133
What clinical signs may suggest immunodeficiency?
Recurrent infections, unusual infections, poor response to treatment, or infections with opportunistic organisms.
134
What is an opportunistic infection?
An infection caused by organisms that normally do not cause disease in healthy individuals.
135
How can immunodeficiency affect immune responses?
It reduces pathogen recognition, immune activation, and pathogen elimination.
136
Why do patients with immunodeficiency often have persistent infections?
Their immune system cannot effectively clear pathogens.
137
What is immune dysregulation?
Failure of the immune system to properly control immune responses.
138
How can immune dysregulation occur in immunodeficiency?
Defective immune control mechanisms allow abnormal immune activity.
139
What is autoimmunity?
A condition where the immune system attacks the body's own tissues.
140
Why can immunodeficiency increase risk of autoimmunity?
Defective immune regulation may allow autoreactive cells to survive.
141
What is hypothyroidism?
A condition where the thyroid gland produces insufficient thyroid hormones.
142
What is the most common autoimmune cause of hypothyroidism?
Hashimoto’s thyroiditis.
143
What happens to the thyroid gland in Hashimoto’s thyroiditis?
Immune cells attack and gradually destroy thyroid tissue.
144
Which antibodies are commonly present in Hashimoto’s thyroiditis?
Anti‑thyroid peroxidase (TPO) and anti‑thyroglobulin antibodies.
145
How can immune dysfunction contribute to hypothyroidism?
Autoimmune destruction of thyroid tissue reduces hormone production.
146
What symptoms are common in hypothyroidism?
Fatigue, weight gain, cold intolerance, constipation, and dry skin.
147
How is immunodeficiency investigated clinically?
Through blood tests measuring immune cells, antibodies, and immune function.
148
Which lab test measures antibody levels?
Serum immunoglobulin measurement.
149
Which test measures immune cell numbers?
Full blood count and lymphocyte subset analysis.
150
Why is it important to distinguish primary from secondary immunodeficiency?
Because the underlying causes, treatments, and prognosis differ.
151
What treatments may be used for immunodeficiency?
Antibiotics, immunoglobulin replacement therapy, immune‑modulating drugs, or stem cell transplantation.
152
Why is early diagnosis of immunodeficiency important?
Early treatment can prevent severe infections and long‑term complications.
153
What are the three main types of muscle tissue?
Skeletal muscle, cardiac muscle, and smooth muscle.
154
Which muscle type is voluntary?
Skeletal muscle.
155
Which muscle types are involuntary?
Cardiac muscle and smooth muscle.
156
What is the main function of skeletal muscle?
Voluntary movement, posture maintenance, and heat production.
157
What is the main function of cardiac muscle?
Pumping blood through rhythmic contraction of the heart.
158
What is the main function of smooth muscle?
Regulating movement within hollow organs and blood vessels.
159
Where is skeletal muscle found?
Attached to bones via tendons.
160
Where is cardiac muscle found?
In the walls of the heart (myocardium).
161
Where is smooth muscle found?
In walls of hollow organs such as intestines, blood vessels, bladder, and uterus.
162
What is a muscle fibre?
A single elongated muscle cell.
163
What is the sarcolemma?
The plasma membrane of a muscle cell.
164
What is the sarcoplasm?
The cytoplasm of a muscle cell.
165
What are myofibrils?
Contractile structures within muscle fibres composed of repeating sarcomeres.
166
What is a sarcomere?
The basic contractile unit of striated muscle.
167
What proteins form the thick filaments in muscle?
Myosin.
168
What proteins form the thin filaments in muscle?
Actin.
169
What regulatory proteins are found on actin filaments?
Troponin and tropomyosin.
170
What is the role of tropomyosin?
It blocks myosin binding sites on actin when muscle is relaxed.
171
What is the role of troponin?
It binds calcium and moves tropomyosin to expose myosin-binding sites.
172
What are the striations in skeletal and cardiac muscle?
Alternating light and dark bands caused by the arrangement of actin and myosin.
173
What are the A bands?
Dark bands containing thick filaments (myosin).
174
What are the I bands?
Light bands containing only thin filaments (actin).
175
What is the Z line?
Boundary between sarcomeres where actin filaments anchor.
176
What is the sliding filament theory?
Muscle contraction occurs when actin filaments slide past myosin filaments, shortening the sarcomere.
177
What triggers skeletal muscle contraction?
A nerve impulse from a motor neuron.
178
What is the neuromuscular junction?
The synapse between a motor neuron and a skeletal muscle fibre.
179
Which neurotransmitter is released at the neuromuscular junction?
Acetylcholine.
180
What happens when acetylcholine binds receptors on the muscle cell?
It triggers depolarisation of the muscle membrane.
181
What structure stores calcium in muscle cells?
The sarcoplasmic reticulum.
182
Why is calcium important in muscle contraction?
It binds troponin and allows actin–myosin interaction.
183
What provides energy for muscle contraction?
ATP.
184
What happens during the cross-bridge cycle?
Myosin heads attach to actin, pull the filament, detach, and repeat using ATP.
185
What happens to calcium during muscle relaxation?
It is pumped back into the sarcoplasmic reticulum.
186
How does cardiac muscle differ structurally from skeletal muscle?
Cardiac muscle cells are shorter, branched, and connected by intercalated discs.
187
What are intercalated discs?
Specialised junctions connecting cardiac muscle cells for coordinated contraction.
188
What types of junctions are found in intercalated discs?
Gap junctions and desmosomes.
189
What is the function of gap junctions in cardiac muscle?
They allow electrical signals to spread between cells.
190
Why does cardiac muscle contract rhythmically?
It has intrinsic pacemaker cells that generate electrical impulses.
191
Which structure normally acts as the heart’s pacemaker?
The sinoatrial (SA) node.
192
How does smooth muscle differ from skeletal muscle?
Smooth muscle lacks striations and sarcomeres.
193
What is the shape of smooth muscle cells?
Spindle-shaped with a single central nucleus.
194
How does smooth muscle contraction differ from skeletal muscle contraction?
It uses calcium and calmodulin to activate myosin rather than troponin.
195
What protein binds calcium in smooth muscle?
Calmodulin.
196
What enzyme is activated by the calcium–calmodulin complex?
Myosin light-chain kinase (MLCK).
197
What is the function of smooth muscle in blood vessels?
Regulates vessel diameter and blood pressure.
198
What is peristalsis?
Wave-like contractions of smooth muscle that move food through the digestive tract.
199
What is muscle fatigue?
A decline in muscle’s ability to generate force.
200
What causes muscle fatigue?
ATP depletion, ion imbalance, and accumulation of metabolic byproducts.
201
What is muscular dystrophy?
A group of genetic diseases causing progressive skeletal muscle weakness.
202
What protein is defective in Duchenne muscular dystrophy?
Dystrophin.
203
Why is dystrophin important?
It stabilizes muscle cell membranes during contraction.
204
What is myasthenia gravis?
An autoimmune disease where antibodies attack acetylcholine receptors at the neuromuscular junction.
205
What symptom is characteristic of myasthenia gravis?
Muscle weakness that worsens with activity.
206
What is hypertrophic cardiomyopathy?
A disease where heart muscle becomes abnormally thick.
207
Why is hypertrophic cardiomyopathy dangerous?
It can impair cardiac function and cause arrhythmias.
208
What happens when smooth muscle in airways contracts excessively?
Airway narrowing as seen in asthma.
209
What type of muscle tissue is this?
skeletal:
- straited (visible sarcomeres)
- multi nucleated
- long cylindrical fibres
210
What type of muscle tissue is this?
smooth muscle:
- not striated
- only one centrally located nucleus
- fusiform/ spindle shaped
211
What type of muscle tissue is this?
cardiac muscle:
- striated
- one/two central nuclei
- short branched fibres
- intercalated discs
