workshop test 1 Flashcards
- Describe the hypothalamic-pituitary-thyroid axis feedback mechanism (3 marks).
- Hypothalamus releases TRH.
- TRH stimulates the anterior pituitary gland to release TSH.
- TSH then stimulates the thyroid gland to produce thyroid hormones (T3 and T4)
- High levels of thyroid hormones (T3 and T4) inhibit release of TRH and TSH (negative feedback loop)
- Describe the levels of Thyroid hormone (TH) and thyroid stimulating hormone (TSH) you would expect to see in a patient with Graves’ disease with reference to the feedback loop and the general effect of hyperthyroidism on the body (5 marks).
- If have graves’ disease
- TH levels: Increased levels of TH due to thyroid gland being overactive.
- TSH levels: Suppressed/decreased levels of TSH due to negative feedback loop producing excess TH.
- Effect on body: increased heart rate and force of contraction, goitre (enlarged thyroid gland due to increased TH), increased metabolic heat production.
- Discuss the rationale for Jim’s diabetes, the actions of insulin and how these actions relate to Jim’s symptoms (7 marks).
- Jim most likely has type 1 diabetes
- Which is the result of a loss of pancreatic b-cells due to an auto-immune response which causes the destruction of b-cells
- Insulin function: facilitates glucose uptake into cells, increasing blood glucose levels as insulin remains in blood, increasing risk of hyperglycaemia
- Jim’s symptoms: constant hunger and fatigue =because body can’t take up glucose, weight loss due to dehydration loss of fluid, significant weight loss = due to dehydration- loss of fluid, use of fat and protein as energy source, increased urination= due to due to dehydration as there’s osmotic effects of high glucose excreted in the urine.
- If Jim is diagnosed with diabetes, what would you expect to see in the blood and urine samples (1 mark).
- Blood: Expect to see high blood glucose levels in blood (hyperglycaemia)
- Urine: expect to see presence of glucose
- Discuss the changes in CRH, ACTH and cortisol secretion that you would expect to see in this patient (with Cushing’s disease). Using your knowledge of cortisol regulation, explain why you would see these changes and the symptoms the patient is experiencing (8 marks).
- CRH: there would result in increased CRH released from the hypothalamus.
- ACTH: due to increase in CRH, the anterior pituitary gland will stimulate release of more ACTH.
- Cortisol: increased cortisol levels due to ACTH stimulating increased secretion from the adrenal cortex.
- Increased ACTH inhibits CRH release + increased cortisol inhibits CRH release and ACTH release.
- Hyperglycaemia= due to gluconeogenesis (increased glucose bc of cortisol), and increased fat deposition in the face and trunk and wasting of the limbs is due to protein catabolism and lipolysis. (all because of increased cortisol from hypercortisolism)
- Describe how the structure of a lymph node allows lymphocytes and macrophages to perform their protective function (4 marks)
- Lymph node has a subcapsular sinus which allows lymph fluid to flow through to the medulla and the cortex.
- The cortex part of the lymph node has lyphoid follicles which are rich in B lymphocytes, where B cells are activated and mature.
- The medulla part is where the macrophages and plasma cells are located, where lymph is further filtered and antibodies are released.
- The macrophages will undergo phagocytosis where they’ll engulf pathogens when they filter lymph
- The Lymphocytes will initiate immune response, via an adaptive immune response.
- In which regions of the body would lymphadenopathy be most visible, explain your answer (4 marks)
Cervical areas, axillary areas in the armpits and inguinal (groin) regions. These places contain lost of lymph nodes which are located near lymphatic drainage sites. They would therefore be places where the lymph nodes commonly swell, resulting in more lymph filtered an immune responses occurring.
- Describe how the process of inflammation aids in the immune response against the virus (3 marks).
- Vasodilation: as there’s increased blood flow in capillaries, this will bring more immune cells to the site of infection,
- Increasing membrane permeability as allows immune cells (like dendritic cells) to enter the infected tissue and undergo an immune response.
- Symptoms: resulting in swelling, redness and heat which help isolate the infection.
- Explain why you never experience symptoms referring to clonal selection and immunological memory (5 marks).
- Clonal selection: during first infection, specific immune cells recognise the viruses’ antigens on the immune cells (T helper cells and B cells) MHC 2 markers, and multiply rapidly via clonal differentiation and expansion.
- Memory cell formation: some of these cells become memory cells that remain in body after infection.
- Re-infection: when viral antigen is exposed again, memory cells recognise the virus’ antigen and responds faster than first infection, producing antibodies to help neutralise virus (if a b cell), and if T cell activate other cells such as T cytotoxic cells, they release cytotoxic chemicals to also neutralise the cell or activate other immune cells.
- Immunological memory: due to memory cells formed, more rapid response to prevent symptoms.
- Describe the differences between the organisation and function of the hypothalamus & posterior pituitary gland, vs the hypothalamus and anterior pituitary gland. Make general references to how hormones are released in each part of the pituitary gland and how the hypothalamus controls this release (4 marks).
Posterior Pituitary
- Stores and releases hormones (such as ADH and oxytocin) that are produced in the hypothalamus.
- The hormones travel down the axons to the terminals, where they are stored and released into general circulation via the capillary plexus of the hypophyseal veins of the posterior pituitary when needed.
Anterior Pituitary
- Produces and secretes its own hormones (e.g. TSH and ACTH) in response to signals from the hypothalamus.
- The hypothalamus releases specific hormones into the blood capillaries (primary plexus of the hypophyseal portal system) where they travel down portal veins into the secondary plexus into the anterior pituitary where hormone production and secretion is regulated.
Control summary:
Posterior: controlled by neural connections from hypothalamus
Anterior: controlled by hormonal signals from hypothalamus, which allows for regulated hormonal output.
- What are the general mechanisms of action that make antibodies a key component of an immune response (4 marks)?
- Neutralization: Antibodies bind to pathogens, blocking their ability to infect cells.
- Opsonization: Antibodies mark pathogens for phagocytosis by macrophages.
- Agglutination: Clumping pathogens together, making them easier to eliminate.
- Complement Activation: Antibody binding to complement pathogen triggers the complement system, leading to pathogen lysis.
- Describe the interaction between macrophages and T lymphocytes during the presentation of antigen (4 marks).
The interaction between macrophages and T lymphocytes during antigen presentation is a
critical component of the immune response. Macrophages act as antigen-presenting cells
(APCs) by engulfing pathogens and processing them into antigenic peptides. These peptides
are then presented on the surface of macrophages bound to major histocompatibility
complex (MHC) molecules. T lymphocytes, specifically CD4+ helper T cells, recognise these
MHC-antigen complexes through their T cell receptors (TCRs). This recognition is the first
signal required for T-cell activation. For full activation, a second co-stimulatory signal is
needed, which is provided by the interaction of additional molecules on the macrophage
surface, such as CD80/CD86, with receptors on the T cell, like CD28. Once activated, T cells
proliferate and differentiate into effector cells, which can help orchestrate the immune
response, or into memory cells, which provide long-term immunity. This interaction ensures
that T cells are specifically activated in response to the presence of a pathogen, facilitating a
targeted immune response.
