Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > Exam V Comprehensive > Flashcards

Exam V Comprehensive Flashcards

1
Q

Where are the voltage-gated Na+ channels on myelinated nerves?

A

Nodes of Ranvier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Difference between myelinated and unmyelinated nerves – which conducts more rapidly? more efficienctly?

A
  • -Myelinated – salutatory conduction: don’t waste time generating action potential’s between nodes
  • -Myelinated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does the following diseases or toxins affect synaptic transmission? pre- or post-synaptic? autoimmune disease or no? – myasthenia gravis

A
  • -POST-synaptic
  • -reduces the number of ACh receptors at the postsynaptic neuromuscular junction; because there are less functional nicotinic acetylcholine receptors, the end-plate potential is smaller than normal; if the EPP is too small, the skeletal muscle cell will not generate an action potential, causing muscle weakness and even muscle paralysis
  • -autoimmune disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does the following diseases or toxins affect synaptic transmission? pre- or post-synaptic? autoimmune disease or no? – Eaton-Lambert syndrome

A
  • -PRE-synaptic
  • -usually caused by autoimmune attack on voltage-gated Ca++ channels in the terminals of somatic motor nerves; can occur in patients with certain types of cancer especially small cell carcinoma of the lungs
  • -autoimmune disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does the following diseases or toxins affect synaptic transmission? pre- or post-synaptic? autoimmune disease or no? – botulinum toxin

A
  • -PRE-synaptic disorder
  • -clostridial toxins are highly specific proteases that cleave certain synaptic proteins, which interferes with the release of NT at the neuromuscular junction; conditions include focal dystonia, strabismus, and facial wrinkles
  • -NOT autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does the following diseases or toxins affect synaptic transmission? pre- or post-synaptic? autoimmune disease or no? – α-bungarotoxin

A
  • -POST-synaptic
  • -peptide from venom of banded krait, irreversibly blocks nAChR
  • -NOT autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What NT do all somatic nerves release?

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What NT do all preganglionic fibers in the ANS release?

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What NT do parasympathetic post-ganglionic fibers release?

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What NT do sympathetic post-ganglionic fibers release?

A

They are adrenergic (Epi/NE) or dopaminergic (dopamine – renal vascular smooth muscle)
–thermoregulatory sweat glands are exception (muscarinic receptors to respond to ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dual innervation: what is it? exceptions?

A
  • -The actions of most organs are controlled by both sympathetic and parasympathetic innervation because they receive innervation from both
  • -Exceptions: only sympathetic = hair follicles, sweat glands, liver, adrenal glands, kidneys, blood vessels; salivary glands have same effect from both PNS and SNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cholinergic neurotransmission: synthesis

A

Choline is transported from the extracellular fluid into the neuron terminal by a sodium-dependent membrane choline transporter (CHT); can be inhibited by a group of drugs called the hemicholiniums

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cholinergic neurotransmission: storage

A

ACh is transported into the storage vesicle by a second carrier, the vesicle-associated transporter (VAT); can be inhibited by vesamicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cholinergic neurotransmission: release

A

Calmodulin interacts with the VAMP synaptotagmin on the vesicle membrane and triggers fusion of the vesicle membrane with the terminal membrane and opening of a pore into the synapse; the acetylcholine vesicle release process is blocked by botulinum toxin through the enzymatic removal of two amino acids from one or more of the fusion proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cholinergic neurotransmission: termination

A

Acetylcholine’s action is usually very rapidly terminated via metabolism by the enzyme acetylcholinesterase; pharmacological blockade of acetylcholinesterase with drugs such as neostigmine enhances acetylcholine effects and is used both in medicine and in industry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Adrenergic neurotransmission: synthesis

A

Catecholamines are derived from tyrosine via the rate limiting step of the enzyme tyrosine hydroxylase; this is inhibited by tyrosine analog metyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Adrenergic neurotransmission: storage

A

Synthesized catecholamines are transported into vesicles by the vesicular monoamine transporter (VMAT); can be inhibited by the reserpine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Adrenergic neurotransmission: release

A

Same as ACh (calmodulin interacts with the VAMP synaptotagmin on the vesicle membrane and triggers fusion of the vesicle membrane with the terminal membrane and opening of a pore into the synapse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Adrenergic neurotransmission: termination – simple diffusion

A

Catecholamines diffuse into the circulation and are metabolized by catechol-O-methyltransferase (COMT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Adrenergic neurotransmission: termination – reuptake

A
  • -Neuronal reuptake: Catecholamines are taken up at nerve terminals by solute carriers. For norepinephrine, the transporter is norepinephrine transporter, NET, which can be inhibited by cocaine and tricyclic antidepressant drugs
  • -Extraneuronal reuptake: extraneuronal can also take up catecholamines via extraneuronal transporters (ENT) (also called NET2); a number of pharmacological agents can inhibit ENT/NET2, such as corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Smooth vs. skeletal muscle: contractile elements

A

Both have actin, myosin, and tropomyosin, but smooth muscle does NOT express troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Smooth vs. skeletal muscle: myosin

A

Myosin heads are not all arranged in same direction in smooth muscle to allow for multi-directional contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Smooth vs. skeletal muscle: dense bodies vs. Z discs

A

Dense bodies: structural proteins disbursed throughout cell that can serve to anchor adjacent cells to each other to allow for contraction to be transmitted
Z discs: pulls skeletal muscle together for contraction to be transmitted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Smooth vs. skeletal muscle: actomyosin regulation

A

Smooth muscle has NO troponin and myosin is arranged differently

25
Q

How does calcium participate in smooth muscle mechanical and electrical events?

A
  • -Extracellular fluid = primary source of calcium; Ca++ plays a very important role in both depolarization of the membrane and activating the contractile process, once bound to calmodulin.
  • -Intracellular calcium from the sarcoplasmic reticulum also plays a role; however, the SR is not as well developed as seen in skeletal muscle and therefore does not serve as a primary source of calcium for the contractile process
26
Q

Flow, velocity of flow, and surface area through vascular system

A
  • -Volume of flow is equal at all levels
  • -As total cross sectional area increases (arteries to arterioles), the flow velocity decreases; flow is proportional to pressure gradient, the 4th power of the radius and inversely proportional to viscosity and length of the capillary; radius has a great impact on the flow (increase radius –> greater flow)
  • -Capillaries have the maximum surface area with the minimum velocity
27
Q

Relationships between flow, pressure, and resistance

A

Flow = (Pi-Po )/Resistance

28
Q

Parameters that need to be known to calculate total peripheral resistance and resistance of pulmonary circuit

A

Total peripheral resistance: Pi=aortic pressure, Po=right atrial pressure, CO
Pulmonary circuit resistance: Pulmonary artery pressure, left atrial pressure, CO
—TPR=(Pi-Po)/(CO)

29
Q

Temperature-induced changes in heat loss when anterior hypothalamus is activated

A

Cutaneous dilation occurs, which is mediated by decreased adrenergic tone (decreased norepinephrine), which is decreased activation of α1 receptors. Cutaneous blood flow represents the exception to the rule for control, which is normally that organs control their blood flow according to local factors and events, and don’t pay attention to the brain.

30
Q

Thermoregulatory sweating

A

Sympathetic cholinergic event: muscarinic receptors are activated on merocrine sweat glands; anxiety sweating results from sympathetic adrenergic stimulation of a few sweat glands that have α1 receptors; apocrine sweat glands which are in the axillary region are regulated by sympathetic adrenergic control; muscle tone is inhibited, therefore shivering is inhibited – inhibition of chemical thermogenesis will occur

31
Q

Exposure to cold – mechanisms for heat gain

A

Posterior hypothalamus is activated. There is cutaneous vasoconstriction with increased sympathetic tone and alpha one activation; piloerection, “goosebumps” – erector pilli muscles will be activated via α1 receptors and increased sympathetic tone; these are attached to cutaneous hair follicles; shivering is mediated by primary motor center for shivering in the posterior hypothalamus

32
Q

Sympathetic chemical thermogenesis

A

Norepinephrine and epinephrine stimulate brown fat, which produces heat by oxidative phosphorylation but doesn’t produce ATP; sympathetic activation via β1 receptors, possibly β3

33
Q

How are thyroid hormones involved in temperature regulation?

A

Increase the cellular metabolism and heat production

34
Q

Glycoproteins involved in platelet adhesion and activation

A

GPIbα: von Willebrand Factor (vWf)
GPVI: Collagen
GPIIa/IIIb: Fibrinogen

35
Q

G protein-coupled receptors involved in platelet adhesion and activation

A

P2Y12: ADP
Protease activated receptor (PAR): Thrombin
Thromboxane A2 receptor: Thromboxane A2

36
Q

Function of platelet-secreted ADP

A

Further activate platelets

37
Q

Function of platelet-secreted serotonin

A

Further activate platelets and to cause vasoconstriction

38
Q

Function of platelet-secreted thromboxane A2

A

Further activate platelets and to cause vasoconstriction

39
Q

Muscles of inspiration/how they move

A
  • -Diaphragm – moves downward to create negative pressure
  • -External intercostals – raise rib cage
  • -Scalenes and sternocleidomastoids – raise 1st and 2nd ribs (NOT visible normally)
40
Q

Muscles of expiration/how they move

A
  • -Abdominal wall muscles – force diaphragm upward

- -Internal intercostals – lower rib cage

41
Q

Definition and clinical uses of FVC

A

Forced Vital Capacity (FVC): total amount of air that can be forcibly expired after max inspiration

42
Q

Definition and clinical uses of FEV1

A

Forced Expiratory Volume in first second of exhalation

43
Q

Definition and clinical uses of FEV1/FVC ratio

A

Reflects resistance to airflow (should be about 0.8)

44
Q

Definition and clinical uses of FEF25-75

A

Flow rate at 25-75% of exhaled vital capacity – diagnosis and assessment of lung therapy

45
Q

Differences between obstructive and restrictive lung disease (based on numerical changes)

A

Obstructive: both values lower but FEV1 more reduced –> decreased ratio (ex. asthma)
Restrictive: both values decreased, FVC more reduced –> INCREASED ratio (ex. alveolar fibrosis)

46
Q

Patterns of flow volume curve in typical diseases

A

SEE PICTURE!!!
Obstructive: expiration is shifted to the left
Upper airway obstruction: expiration and inspiration stop short
Restrictive: same shape as normal but smaller and shifted right

47
Q

Main differences between asthma, chronic bronchitis, and emphysema (reversibility, sputum production, alveolar damage)

A

Asthma: very reversible, no sputum production or alveolar damage
Chronic bronchitis: slightly reversible, high amounts of sputum, slight alveolar damage
Emphysema: not reversible, no sputum production, large alveolar damage

48
Q

Key pulmonary function test abnormalities in obstructive lung disorders

A
  • -Decreased FEV1/FVC ratio
  • -Decreased airflow rates throughout the vital capacity
  • -Residual volume increased drastically
49
Q

Effects of constricting afferent or efferent arteriole on RBF and GFR

A

Afferent arteriole dilation: increased GFR and RBF
Afferent arteriole constriction: decreased GFR and RBF
Efferent arteriole dilation: decreased GFR, increased RBF
Efferent arteriole constriction: increased GFR, decreased RBF

50
Q

How can you increase glomerular hydrostatic pressure?

A

Dilating afferent arteriole and constricting efferent arteriole

51
Q

FGF23 and its effects

A

Peptide hormone that is made by osteoblasts and osteocytes in bone; decreases reabsorption of phosphate (like PTH) and decreases production of calcitriol (opposite of PTH)

52
Q

Relationships between FGF23, PTH and calcitriol and relation to vitamin D

A

1,25-dehydroxy vitamin D is made in the kidney and travels through the bloodstream; increases the absorption of calcium and phosphate in the intestine (most important effect of vitamin D/calcitriol); suppresses PTH synthesis in the parathyroid gland; stimulates fibroblast growth factor 23 (FGF23) secretion by osteoblasts and osteocytes in bone

53
Q

Type I diabetes

A
  • -Due to β-cell destruction and leads to absolute insulin deficiency.
  • -Key genes associated with development of Type 1 are found at the major histocompatibility (MHC) locus
  • -Infiltration of activated T-lymphocytes is key cause of destruction of islet b cells.
  • -Signs & symptoms: polyuria, thirst, blurred vision, weight loss/polyphagia, weakness/dizziness, paresthesias (tingling), level of consciousness
54
Q

Type II diabetes

A
  • -Due to insulin resistance and insulin secretory defect.
  • -Decline in tissue responsiveness to insulin. This can be detected with elevated plasma insulin but normal plasma glucose. May be due to changes in number of insulin receptors and/or affinity of receptors for insulin.
  • -Increase in insulin secretion and b-cell mass can overcome resistance
  • -Signs & symptoms: asymptomatic initially, infections, neuropathy, classic signs of insulin deficiency (occur slower), obesity & metabolic syndrome
55
Q

Common therapeutic strategies for Type I diabetes treatment

A

Insulin absolutely required as well as patient education and diet change

56
Q

Common therapeutic strategies for Type II diabetes treatment

A

Diet change and patient education, insulin use when other agents, diet, and exercise do NOT allow for achievement of therapeutic goals; may be able to increase insulin secretion, increase insulin action, inhibit gluconeogenesis, and suppress glucagon secretion

57
Q

Hypoglycemia as a side effect of treatment of DM

A

Most common acute complication of those taking insulin or agents that promote insulin secretion

  • -Symptoms produced by ANS: tachycardia, sweating, tremors, nausea, and hunger
  • -Treatment includes glucose or glucagon
58
Q

Diabetic ketoacidosis (DKA) as a side effect of DM

A

Insulin deficiency causing mobilization of energy stores which includes ketogenesis and a resulting metabolic acidosis.

  • -Symptoms produce hyperglycemia and a blood pH lower than 7.0
  • -Treatment goals: restore plasma volume, reduces glucose, correct acidosis, and replenish electrolytes

Physiology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions