Test 1 clinical applications/Investigations Flashcards

1
Q

MMP stands for what?

What is the normal function of MMP:

A

Matrix metalloproteinases

Tissue remodeling (embryonic development and cell migration of phagocytic cells and other WBCs)

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2
Q

What stops matrix metalloproteinases from degrading intracellular proteins?

A

MMPs are activated extracellularly

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3
Q

How can MMPs contribute to disease?

What exists to stop these?

A

MMPs can contribute to disease by helping tumors metastasize and invade different locations. They can also contribute to disease if activated inappropriately.
MMPs are inhibited by
TIMPs

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4
Q

What are some generic examples of diseases that MMPs may be involved in?

A

Cancer migratino
Destruction of Cartilage protein in arthritis
Cardiovascular and neural disease (from an imbalance in TIMPs and MMPs)

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5
Q

Hemodialysis:

Peritoneal dialysis:

A

Hemodialysis: Blood is channeled to an external filtering system
Peritoneal dialysis: a dialysate is introduced into the peritoneal cavity, where the peritoneal membrane serves as the semipermeable membrane.

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6
Q

Dialysate:

A

Net diffusion of waste molecules from blood into the dialysate (the fluid it is diffused into)

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7
Q

What necessitates dialysis?

A

Inability of the kidney to filter (kidney/renal failure)

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8
Q

What are the symptoms of cystic fibrosis:

A

Excessively salty sweat, mucous build up in the pancreas and lung (promoting pancreatic and pulmonary disorders)

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9
Q

What is the molecular cause of cystic fibrosis:

A

A genetic defect in a glycoprotein known as CFTR (cystic fibrosis transmembrane conductance regulator) causes it to not be placed in the golgi complex for processing, and is incorrectly inserted into the plasma membrane

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10
Q

Are all cases of cystic fibrosis equally severe?

Is the disease curable/treateable?

A

Different mutations cause CFTR gene which can have cystic fibrosis of differing severity.
It is not curable but it is treatable.

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11
Q

Why are plasma proteins concentrated in the bloodstream?

What results if there is an abnormally low level of plasma proteins?

A

They cannot exit through the capillary pores, they are therefore osmotically active
The osmotic pressure from plasma proteins draws fluid from the interstitial fluid into the blood. Without this osmotic pressure edema occurs.

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12
Q

What underlying condition may cause there to be inadequate levels of protein in the blood and edema?

A

Cirrhosis of the liver can stop it from producing albumin. As albumin is osmotically active, it causes a drop in the osmolality of the blood and a flow of water into the interstitial fluid (edema)

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13
Q

What is in Ringer’s lactate:

A

Lactate, and Na, Cl, K, and Ca

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14
Q

Why is mannitol sometimes given intravenously to patients in the hospital?

A

Mannitol is osmotically active, and it will draw fluid out of other tissues. This can stop cerebral edema for example.

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15
Q

Why does hyperglycemia (as seen in diabetes mellitus) cause glycosuria

A

Sugar normally enters the urine and is pumped out by Na+/Glucose symport pumps. In patients with hyperglycemia these pumps become saturated and cannot pump out all the glucose in the urine.
Their transport maximum (Tm) is exceeded.

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16
Q

Why does hypoglycemia result in symptoms of the brain getting inadequate glucose?

A

Glucose transport into the brain, is a facilitated transport using GLUT1 and GLUT3 transporters, it relies on the concentration gradient.

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17
Q

What can cause severe hypoglycemia?

What results from severe hypoglycemia

A

Insulin overdose

Failure of glucose to diffuse into the brain. Loss of consciousness or death can ensue.

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18
Q

What are the resulting conditions from acute gastroenteritis:

A

Diarrhea produces loss of Na+ and water, malnutrition, and metabolic acidosis. Kills 1.5 - 2.5 million deaths.

19
Q

ORT: what does it stand for and what is it.

A

Oral rehydration therapy
Na+ and glucose symport into the intestine pulls water into the body through osmosis. A solution of 245 mOsm, Na+ and glucose should be in equal concentration for ideal cotransport conditions to occur.

20
Q

What is the normal plasma K+ concentration?
What concentration can stop the heartbeat?
Why?

A

3.5 to 5.0 mEq/L
> 8 mEq/L
Depolarization of cells (lower resting membrane)

21
Q

Hypokalemia effect on the body:

A

hyperpolarization of cells, cells are harder to activate resulting in slowing down of muscles and nervous system. Weakness and fatigue. Irregular large U wave, inverted T wave

22
Q

What two categories of demyelinating disease:

A

Targeting the CNS: Multiple sclerosis

Targeting the PNS: Guillain-Barre syndrome

23
Q

Guillain-Barre syndrome:

A

T cells attack the myelin sheaths of the PNS. Rapid onset of symptoms, such as muscle weakness (which can cause respiratory failure), autonomic axons also cause issues in blood pressure and cardiac regulation as they are demyelinated

24
Q

Multiple Sclerosis:

  • Description:
  • Target population:
  • Treatment:
A
  • Description:
    Attack mediated by T cells on the myelin sheaths of the CNS. Leading to areas of hardening (sclerosis) followed by degeneration. Chronic relapsing disease with variable symptoms, such as sensory impairments, motor disfunction, and difficulty with bladder and fatigue
  • Target population:
    Manifests ages 20 - 40 twice as prevalent in females
  • Treatment:
    Drugs which decrease autoimmune activity and drugs which interfere with the entry of T cells in the CNS. Help with symptoms but do not restore myelin sheaths or cure disease
25
Q

What mechanism do local anesthetics utilize:

A

They reversibly bind voltage gated Na+ channels and prevent action potentials

26
Q

What was the first local anesthetic:

What else was used as alternative anesthetics:

A

Cocaine

Procaine, Lidocaine

27
Q

Procaine, lidocaine and others like them often have what other type of drug with them? Why?

A

A vasopressor such as epinephrine

Procaine and lidocaine cause vasodilation which limit their usefulness, epinephrine reverses this

28
Q

What is the mechanism of action of Botulinum toxin:

A

Digests (botulinum toxin is a protease) SNAP-25 in excitatory synapses which release Acetylcholine.

29
Q

What is the result of botulinum toxins actions:

A

flaccid paralysis, muscles are unable to react. small amounts of this toxin in botox treatments smooth wrinkles.

30
Q

What is the mechanism of action of tetanus toxin:

A

Targets inhibitory synapses, such as glycine and GABA by digesting synaptobrevin-2.

31
Q

What is the result of tetanus toxin actions:

A

muscle rigidity, and spastic paralysis

32
Q

Myasthenia gravis:

  • What is it:
  • Symptoms:
  • How is it treated:
A
  • What is it:
    autoimmune disease which inactivates Ach receptors in the motor end plate
  • Symptoms:
    Muscle weakness, particularly in the eyes, eyelids and face
  • How is it treated:
    Neostigmine and other drugs which block acetylcholinesterase treats symptoms
33
Q

Neostigmine treats what disorder:

A

Myasthenia gravis

34
Q

Saxitoxin:

  • Mechanism of action:
  • Source:
  • Cause of death:
A
  • mechanism of action:
    Binds to and inactivates voltage gated Na+ channels
  • Source:
    dinoflagellates which become concentrated in filter-feeding clams and mussels
  • Cause of death:
    Diaphragm paralysis
35
Q

Tetrodoxin:

  • Mechanism of action:
  • Source:
  • Cause of death:
A
- Mechanism of action:
Binds to and inactivates voltage gated Na+ channels
- Source:
Puffer fish
- Cause of death:
Diaphragm paralysis
36
Q

Cholinesterase inhibitors:

  • Mechanism:
  • Medicinal application:
  • War and agricultural use:
A
  • Mechanism:
    Inhibit cholinesterase (acetylcholinesterase)
  • Medicinal application:
    Neostigmine and other medicines use this to combat low AcH levels for disorders like myasthenia gravis
  • War and agricultural use:
    Nerve gas kills by inhibiting AChE and therefore overstimulating cholinergic synapses
    Organophosphate pesticides also kill by inhibiting AChE and therefore overstimulating cholinergic synapses
37
Q

Monoamine oxidase define:

A

This is a enzyme in presynaptic cells which breaks down monoamines (dopamine, norepinephrine, serotonin)
There is a transporter which transports monoamines back into the presynaptic cell for destruction

38
Q

Monamine oxidase inhibitors:

  • What they do:
  • Result:
  • Disorders treated:
A
  • What they do:
    deactivate monoamine oxidases
  • Result:
    Rise in monoamines at the synapse (dopamine, melatonin, serotnin, norepinephrine being an example)
  • Disorders treated:
    Depression, anxiety, panic disorder, and Parkinson’s disease.
39
Q

What can go wrong as a result of treatment with MAOIs?

A

The body cannot break down certain amino acids high in monoamines such as tyramine (derived from tyrosine, the source of catecholamines such as dopamine, norepinephrine, and epinephrine) and Tryptophan (the molecule from which serotonin is derived).
Consumption of these foods results in increased norepinephrine released by sympathetic axons increasing heart rate and driving up blood pressure (hypertensive crisis: extremely high blood pressure).

40
Q

Mesolimbic dopamine system is currently associated with what?

A

Reward and behavior

41
Q

Cocaine:

- Mechanisms of action:

A
  • Mechanisms of action:
    Blocks reuptake of dopamine, serotonin and norepinephrine.
    Blocks membrane Na+ channels
42
Q

What does stimulus by cocaine activate?

A

Mesolymbic dopaminic pathway (mesolymbic reward pathway) this results in increased dopamine in the reward pathway, and happy people.

43
Q

What are the negative side-effects of cocaine?

What would the ideal cocaine be like?

A

Restricts coronary arteries, raises cardiac rate and blood pressure (norepinephrine sympathetic innervation?), promotes heart disease, stroke, seizures and ulcers.

It would block reuptake of only dopamine, and only in the mesolymbic dopamine pathway.