FOM Mechs Flashcards

1
Q

haemostasis

A

1.Vascular spasm to reduce blood flow/vasoconstriction
2.Platelet plug formation via adhesion of platelets to temporarily seal the injury.
3.Activation of the coagulation cascade (intrinsic and extrinsic pathways) leading to fibrin clot formation (fibrinogen converted to fibrin)
4.Clot retraction and tissue repair to heal the vessel.
5.Healthy tissue release messengers for Fibrinolysis to remove the clot once it is no longer needed, preventing excess bleeding or unnecessary clotting (homeostasis)

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2
Q

haematoposeis

A

-low RBC count
-hypoxia
-hypoxia detected by kidneys
-kidneys release erythropoietin
-this stimulates erythropoiesis
-increasing RBC count
-oxygen levels increase

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3
Q

Describe how the membrane becomes depolarised and repolarised in cardiac conduction

A

-resting membrane at -70 m/v
-slow influx of Na+ depolarises membrane
-T-type Ca2+ transient channels open and membrane becomes more depolarised
-then Ca2+ L-type channels open and membrane becomes more depolarised
-threshold reached, action potential fired
-K+ channels open, efflux of K+ initiates hyper polarisation

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4
Q

how does the autonomic NS effect heart beat frequency

A

asympathetic (vagal) stimulation increases the K+ efflux and causes hyperpolarisation and slows the depolarisation

-decreased vagal influence, Sympathetic stimulation increases the Ca2+ influx and causes faster depolarisation

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5
Q

Outline what happens in diastole

A

Isovolumetric relaxation (higher pressure in aorta than ventrciles)
 Rapid inflow into ventricles
 Diastasis (reduced inflow into the ventricles)
 Atrial contraction (100% full)
(4 phases)

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6
Q

Outline what happens in systole

A

 Isovolumetric contraction
 Rapid ventricular ejection
 Reduced ventricular ejection
(3 phases)

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7
Q

describe pressure changes in cardiac cycle

A

1.atrial pressure increases as systole is occurring, contraction causes pressure increase
2.AV valves open, blood flow into ventricles, increasing ventricular pressure
3.Ventricles contract, increasing pressure
4.Ventricle pressure>Atrial pressure so AV valves close
5.Ventricle pressure>Aortic pressure so SL valves open
6.ventricle pressure drops as blood leaves ventricle
7.Aortic pressure>Ventricular pressure, SL valves close
8.Ventricular pressure continues to drop until it goes below atrial pressure, left atrium refills (bc AV valves open) and cycle repeats

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8
Q

describe sympathetic innervtion of heart

A

-To increase HR and contractility of the myocardium: cardioacceleratory centre of medulla sends out messages via the sympathetic nerves through the paravertebral ganglion.
-These nerve fibres innervate the SA,AV node and myocardium. -This causes stimulation of adrenal medulla resulting in release of adrenaline and noradrenaline,
-these hormones bind to B1 receptors and cause depolarisation of the nodal cells (threshold is reached) and signals are sent faster, increasing HR and atrial myocardium contractility.

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9
Q

outline baroreceptor reflex

A

1.Change in blood pressure detected by baroreceptors in aortic arch and carotid sinus
2.this sensory (afferent) message is sent to cardioregulatory centres of the medulla (AP sent out faster or slower depending) via afferent cranial nerves (9,10)
3.Cardioregulatory centres send out an efferent message that triggers the sympathetic or parasympathetic NS
4. Changes in CO (SV and HR) and constriction/dilation of blood vessels
5.Increase/decrease in BP

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10
Q

describe parasympathetic innervation of heart

A

-Parasympathetic messages are sent via vagus nerve from dorsal root ganglion to the SA,AV node only (mostly impacts HR)
-Ach is released, which forces efflux of K+, causing hyperpolarisation
-therefore making it harder for HR to increase

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11
Q

gastric mixing

A

-regulated by smooth muscle in walls of stomach
-pacemaker cells generate slow wave potentials
-slow wave potentials set the basic electrical rhythm of the heart
-muscles in wall contract due to slow wave potentials
-these contractions allow for gastric mixing, which in conjunction with gastric juices, which include hydrochloric acid, pepsin, and mucus, mix with the food to form a semi-liquid substance called chyme. The acid helps break down food particles, and pepsin begins the digestion of proteins.

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12
Q

gastric filling

A

-eating triggers the stomach to relax and expands to accommodate the incoming food. This is facilitated by the vagus nerve through a process known as receptive relaxation.
- it also triggers the relaxation of folds within the mucosa (gastric Rugae) in a process called receptive relaxation

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13
Q

gastric emptying

A

-process in which food leaves stomach into small intestine
-regulated by rate at which pyloric sphincter opens
-gastric emptying is influenced by size of meal, presence of nutrients in small intestine, neural and hormonal signals form gut
- The rate of gastric emptying depends on the composition of the chyme. Liquids empty faster than solids, and carbohydrates empty faster than proteins and fats. Fats slow gastric emptying the most due to their longer digestion time and hormonal feedback mechanisms (e.g., release of cholecystokinin).
-Gastric emptying is controlled by neural signals from the enteric nervous system and hormonal signals from the small intestine. The presence of fatty, hypertonic, or acidic chyme in the duodenum triggers the release of hormones such as cholecystokinin, secretin, and gastric inhibitory peptide, which slow gastric emptying.

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14
Q

Outline steps of digestion in duodenum

A

1.fat and protein products in duodenal lumen
2.CCK released from duodenal mucosa
3.CCK is carried by blood into pancreatic acinar cells
4.secretion of pancreatic digestive enzymes into duodenal lumen

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15
Q

outline steps of neutralisation in duodenum

A

1.acid in duodenal lumen
2.secretin released from duodenal mucosa
3.secretin is carried by blood to pancreatic duct cells
4.pancreatic duct sells secrete NaHCO3- solution into duodenal lumen

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16
Q

mechanism of a cough

A
  • Irritant in the respiratory tract
    • Detected by mechanoreceptors
    • These send afferent message to the medulla and pons via the vagus nerve
    • Integrate this information and coordinate a coughing reflex
    • Afferent motor messages sent to respiratory muscles, causing abdomen to contract and the internal intercostals to contract
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17
Q

mechanism of a fever

A
  • Infection/pathogen
    • Endogenous pyrogens released by macrophages and neutrophil
      • IL1 + IL6 + TNF alpha
    • Travel through bloodstream to hypothalamus
    • Hypothalamus releases prostoglandens
    • Increases set temperature of the body
    • This thermo up regulation is achieved through shivering, vasoconstriction
    • Increased body temp provides hostile environment to pathogen and increases WBC activity
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18
Q

Hering breur reflex

A
  • -when lungs become overstretched stretch receptors in the bronchi and bronchioles trasnmit signals through the vagus nerve to DRG
    • -switching off inspiratory signals and preventing further inspiration/prelonging expiration
    • -also increases RR
    • -serves as a protective reflex against over inflation of lungs
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19
Q

erection + orgasm

A

-sexual stimulation
-parasympathetic neuron’s release nitric oxide, this causes dilation of the arteries supplying the penis, thereby increasing blood flow to penis
-increasing pressure of arterial blood entering vascular spaces of erectile tissue compresses the veins of the penis, reducing flow of venous blood away from the penis
-follwoing orgasm sympathetic nerves contract the central artery of the penis and contract smooth muscle around the erectile tissues, which expels blood away from penis

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20
Q

Cell-mediated immunity

A

1.APC’s ingest pathogens and present them on cell via MHC
2.naive T cells recognise MHC via TCR’s and co-stimulatory signals (become activated)
3.T cell undergoes clonal expansion
4.T cells differentiate into Tc cells, Th cells, Treg cells
5.effector T cells migrate to site of infection via chemotaxis guided by chemokine
6.Tc cells recognise and bind to infected cells that display antigen on MHC I
7.Tc cells release cytotoxic chemical eg perforins that lead to apoptosis of infected cell
8.Th cells release cytokines to amplify immune response, attract macrophages, activate B cells
9.some T cells divide into T memory cells for long term immunity
10. Tregs suppress excessive immune response, prevent autoimmunity and maintain homeostasis

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21
Q

Humoral immunity

A

-naive B cell sitting in secondary lymphoid tissue (lymph node)
-when antigen drains into lymph node it recognises a s+c naive B cell
-naive B cell is activated and proliferates to create a clone of itself
-proliferated B cell divides into plasma and memory cells
-plasma cells secrete IgM and memory cells secrete IgG

22
Q

emesis

A

1.coordinated by vomiting centres of medulla in brainstem
2.deep inspiration; glottis is closed uvula raises
3.stomach, oesophagus and gastro-oesophageal sphincter relax
4.respiratory muscles contract, stomach is squeezed between descending diaphragm and increasing intra-abdominal pressure
5.sensation of nausea , salivation , sweating, tachycardia regulated by ANS
6. Excess vomiting results in loss of fluids and acids

23
Q

protein digestion

A

Stomach:

Acidic Environment: Hydrochloric acid (HCl) denatures proteins, making them easier for enzymes to act upon.
Pepsin: An enzyme secreted as pepsinogen by chief cells in the stomach is activated by HCl into pepsin. Pepsin begins breaking proteins down into smaller peptides.

Small Intestine:
Pancreatic Enzymes: The pancreas secretes trypsinogen, chymotrypsinogen, and procarboxypeptidase, which are activated in the duodenum to trypsin, chymotrypsin, and carboxypeptidase. These enzymes further break down peptides into smaller peptides and amino acids.
Brush Border Enzymes: Enzymes like aminopeptidases and dipeptidases on the surface of the intestinal microvilli complete the breakdown of peptides into individual amino acids.

Absorption
Amino Acids and Small Peptides: Absorbed by enterocytes via active transport mechanisms and then transported into the bloodstream.

24
Q

carbohydrate digestion

A

Mouth:

Salivary Amylase: Begins the breakdown of starch (a polysaccharide) into maltose and dextrins (smaller polysaccharides).
Stomach:

No significant carbohydrate digestion: The acidic environment inactivates salivary amylase.
Small Intestine:

Pancreatic Amylase: Secreted by the pancreas into the duodenum, continues the breakdown of starch and dextrins into maltose, maltotriose, and oligosaccharides.
Brush Border Enzymes: Enzymes such as maltase, sucrase, and lactase on the microvilli of enterocytes break down disaccharides (maltose, sucrose, and lactose) into monosaccharides (glucose, fructose, and galactose).
Absorption:

Monosaccharides: Absorbed by enterocytes via active transport (glucose and galactose) or facilitated diffusion (fructose) and then transported into the bloodstream.

25
Q

fat digestion

A

Mouth:

Lingual Lipase: Begins the breakdown of triglycerides into diglycerides and free fatty acids.
Stomach:

Gastric Lipase: Continues the breakdown of triglycerides into diglycerides and free fatty acids. However, the major site of fat digestion is the small intestine.
Small Intestine:

Bile Salts: Secreted by the liver and stored in the gallbladder, emulsify fats into smaller droplets, increasing the surface area for enzyme action.
Pancreatic Lipase: Secreted by the pancreas, it breaks down emulsified triglycerides into monoglycerides and free fatty acids.
Colipase: A protein that binds to the fat droplets, aiding pancreatic lipase action.
Formation of Micelles:

Micelles: Bile salts, monoglycerides, and free fatty acids form micelles, which are small, soluble aggregates that transport lipids to the intestinal mucosa.
Absorption:

Fatty Acids and Monoglycerides: Diffuse into enterocytes. Inside enterocytes, they are re-esterified into triglycerides.
Chylomicrons: Triglycerides are packaged with cholesterol, phospholipids, and proteins into chylomicrons, which are released into the lymphatic system and eventually enter the bloodstream.

26
Q

endospore formation

A

-DNA is replicated
-cellular divison of cytoplasmic membrane
-prespore formation begins
-cortex formation
-spore coat formation begins
-maturation begins exosporium formation
-mother cell releases mature spore

27
Q

+RNA virus replication

A

1.+RNA infects host cell, expresses viral genome; proteins including RdRp are produced and accumulate in cell
2.Once RdRp levels are sufficient, the replication complex is created, RdRp creates -RNA
3.-RNA acts as a template for synthesis of +RNA, this mRNA is utilised by hosts translational machinery

28
Q

-RNA virus replication

A

1.-RNA infects host cell, it caries its own RNA Polymerase enzyme
2.RNA polymerase produces mRNA that codes for viral proteins
3.-RNA is transcribed into +RNA, which is transcribed back into -RNA, this process is viral replication

29
Q

DNA virus replication

A

1.attachment and entry (via mediated endocytosis)
2.Host RNA polymerase transcribes immediate, early and late mRNA
-specific translated proteins replicated viral DNA genome
-capsids are assembled in nucleus and release virions

30
Q

Classic complement pathway

A
  • Complement pathway triggered by complement protein binding to antibody
31
Q

Alternative complement pathway

A
  • Complement is activated without the presence of antibody or lectin
32
Q

Lectin complement pathway

A
  • Complement protein binds a mannose protein to the pathogen
33
Q

Primary immune response

A

1.lag period:first B cell must find its antigen after exposure
2.initial spike of IgM antibodies:plasma cell (IgM) production increases
3.following rise in IgG antibodies: memory B cell (IgG) production increases
4.IgM and IgG antibodies have achieved their function t/f concentrations decrease

34
Q

Secondary immune response

A

1.reduced lag period due to more cloned B memory cells to recognise antigen
2.initial spike of IgG due to B memory cells
3.spike of IgM due to plasma cells (immune response)
4.more B memory cells for priming future exposures

35
Q

Vaccination - first exposure

A

1.the vaccine is introduced to the body and injected under the skin
2.the vaccine is taken up and digested by DC, Toll-like receptors on surface of DC facilitate relocation to secondary lymphoid organs
3.vaccine is processed and presented on MHC II to naive CD4+ cell
4.”line up” of CD4+ cells to find a complementary match
5.activation, proliferation and differentiation into Th cell
6.Th cells activate a B cell that recognises the vaccine
7.B cell activates, proliferates and differentiates, into IgM plasma cell, IgG memory cells
8.clones of B memory cells that can recognise infectious agents

36
Q

Vaccination - second exposure

A

1.antigen is presented on MHC II, proliferation of B cell begins
2.surplus of B cells differentiate into IgM secreting plasma cells and IgG secreting memory cells (tops up memory)

37
Q

Inflammation

A
  1. break in skin/injury introduces bacteria
  2. macrophages engulf the pathogen and release chemotaxins (cytokine)
  3. mast cells activated, release histamine
  4. histamine dilates local blood vessels and widens capillary pores, some cytokines cause neutrophils and monocytes to stick to blood vessel wall
  5. chemotaxins attract neutrophils and monocytes, increased leakiness moves exudate to site of injury
  6. macrophages and neutrophils destroy bacteria
38
Q

Outline, in brief, how hormone secretion from the adrenal gland is regulated

A

-regulated by the hypothalamic-adrenal-pituitary axis (HPA)
-when stressed hypothalamus releases CRH that stimulates anterior pituitary gland to secrete ACTH
-ACTH acts on zona fasciculata which causes release of glucocorticoids, mainly cortisol
-cortisol supports actions of catecholamines in stress response

39
Q

insulin action in proteins

A

-promotes active transport of protein in muscles
-increases protein synthesis

40
Q

insulin action in carbs

A

-facilitates glucose uptake and utilisation (most cells)
-stimulates glycogenesis and inhibits glycogenolysis (liver and muscle)
-increase conversion of glucose into fatty acids (triglycerides) in adipose cells
-inhibits gluconeogeneis (decreasing availability of amino acids and inhibiting hepatatic enzymes)

41
Q

insulin action in fats

A

-increase fatty acid uptake in adipose tissue
-increases fatty acid synthesis from glucose in adipose tissue
-decrease lipolysis in adipose

42
Q

conditioned saliva reflex

A

Receptor: taste receptors on tongue
Afferent nerve: taste fibres of the facial and glossopharangyeal nerve
Control centre: higher centres of the brain including cerebral cortex
Efferent nerves: parasympathetic fibres of facial and glossopharangyeal nerve
Effector: salivary glands
Response: increased saliva secretion

43
Q

describe the simple reflex for increased saliva

A

Receptor: chemoreceptors in the oral cavity
Afferent nerve: glossopharangyeal nerve and trigeminal nerve
Control centre: salivary centres in medulla oblongata
Efferent nerves: parasympathetic fibres of glossopharangyeal nerve
Effector: salivary glands
Response: increased salivary secretion

44
Q

Describe the menstrual phase of female reproductive system in ovaries and in uterus

A

in ovaries: ovarian follicles grow/enlarge
in uterus: stratum functionalis layer of endometrium is degenerated and expelled (menstruation)

45
Q

Describe the pre-ovulatory phase of female reproductive system in ovaries and in uterus

A

in ovaries:
-follicles grown and secrete oestrogen
-one follicle dominates and becomes a tertiary follicle
in uterus:
-oestrogen from ovarian follicles stimulates repair and growth of stratum functionalis in endometrium

46
Q

Describe the ovulatory phase of female reproductive system in ovaries and in uterus

A

in ovaries:
-tertiary follicle ruptures
-secondary oocyte is released into uterine tubule
in uterus
-stratus functionalism continue growing

47
Q

Describe the post-ovulatory phase of female reproductive system in ovaries and in uterus

A

In ovaries:
-remaining follicle becomes corpus luteum
-secretes and oestrogen and progesterone
-luteum can degenerate into albicans
in uterus:
-oestrogen and progesterone from corpus luteum activate uterine glands to secrete mucus

48
Q

Describe the structural changes that occur in the endometrium during menstrual phase and how these changes are controlled by hormones

A

-low levels of progesterone and oestrogen trigger:
-shedding of the functional layer of the endometrium (bleeding)
-endometrium becomes thin and contains mostly blood vessels and stromal cells

49
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49
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