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Points and Channel location > Sridah/ Bio Med Semester 2 Term 1 > Flashcards

Sridah/ Bio Med Semester 2 Term 1 Flashcards

1
Q

Blood

PH:
% plasma :
% Formed elements :
% WBC + Platlets:

A

PH: 7.45

% plasma : 55%

% Formed elements : 45%

% WBC + Platlets: 1%

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2
Q

Functions of Blood

A

Distribution :

oxygen and nutrients

removing metabolic waste via lung and kidney

Transport hormones

Regulation:
Body Temp
PH 7.4
Fluid volume/ salts/proteins

Protection:

WBC for infections , Prevent loss or coagulation/clotting

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3
Q

Plasma and its main protein

A

90% water and 10% solutes

Albumin is 60% plasma protein
Albumin shuttles molecultes (lipid and fats, vitamins, buffers PH Osmotic pressure control

Globulins are 33%

Clotting proteins are 4%

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4
Q

how long do erythrocytes and leukocytes live for?

A

E = 100-120 days
L = 3-4 days

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5
Q

RBC’s

A

flexible spectin inner protien fibers/ concave middle

NO Mitochondia = no Oxygen consumption

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6
Q

Hemoglobin

A

respiratory gas transport

Female : 12-16 g/100ml
Male : 13-18g/100ml

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7
Q

Hematopiesis

A

Blood cell formation

Occurs in the Red bone marrow of

Axil skeleton
epiphysis of the humerus and femur

Hemocytoblasts give rise to all formed elements

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8
Q

Production of Erythrocytes: Erythropoiesis

A

▪ The developmental pathway consists of three phases

▪ Phase 1 – ribosome synthesis in early erythroblasts

▪ Phase 2 – Hb accumulation in late erythroblasts and normoblasts

▪ Phase 3 – ejection of the nucleus from normoblasts and formation of
reticulocytes

▪ Reticulocytes then enter the blood stream and in 2 days become mature
erythrocytes

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9
Q

▪ Too few RBCs leads to tissue ….
▪ Too many RBCs causes undesirable …
▪ Erythropoiesis is hormonally controlled and depends on adequate
supplies of …

A

▪ Too few RBCs leads to tissue hypoxia
▪ Too many RBCs causes undesirable blood viscosity
▪ Erythropoiesis is hormonally controlled and depends on adequate
supplies of iron, amino acids, and B vitamins

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10
Q

Erythropoietin (EPO) release by the …….. is triggered by:

A

Erythropoietin (EPO) release by the kidneys is triggered by:

Hypoxia due to decreased RBCs
▪ Decreased oxygen availability
▪ Increased tissue demand for oxygen
▪ Enhanced erythropoiesis increases the:
▪ RBC count in circulating blood
▪ Oxygen carrying ability of the blood

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11
Q

WBC
Granulocytes …

A

Neutrophils 50-70%
Eosinophils 2-4 %
Basophils 0.5-1%

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12
Q

WBC
Agranulocytes

A

Lymphocytes 25-45%
Monocytes 3-8%

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13
Q

WBC
Granulocytes …

elaborate on them all :

A

Neutrophils are our body’s bacteria slayers
(antibiotic-like
proteins)

Eosinophils
Lead the body’s counterattack against parasitic worms and allergymediated reactions

Basophils :
▪ Histamine – inflammatory chemical that acts as a vasodilator and
attracts other WBCs (antihistamines counter this effect)

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14
Q

Agranulocytes –

A

lymphocytes and monocytes:
▪ Lack visible cytoplasmic granules
▪ Are similar structurally, but are functionally distinct and unrelated cell
types
▪ Have spherical (lymphocytes) or kidney-shaped (monocytes) nuclei

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14
Q

Lymphocytes

A

Are found mostly enmeshed in lymphoid tissue (some circulate in the
blood)
▪ There are two types of lymphocytes: T cells and B cells
▪ T cells function in the immune response
▪ B cells give rise to plasma cells, which produce antibodies

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15
Q

Monocytes

A

Monocytes
They leave the circulation, enter tissue, and differentiate into
macrophages

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16
Q

Macrophages

A

▪ Macrophages: derived from monocytes
▪ Are highly mobile and actively phagocytic
▪ Activate lymphocytes to mount an immune response

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17
Q

Leukocyte Disorders

A

▪ Overproduction = leukocytosis
▪ Underproduction = leukopenia
▪ Leukemias = “White Blood”
▪ Myelocytic
▪ Lymphocytic

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18
Q

Platelets

A

Their granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived
growth factor (PDGF)

▪ Platelets function in the clotting mechanism by forming a temporary plug
that helps seal breaks in blood vessels

▪ Platelets not involved in clotting are kept inactive by NO and prost

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19
Q

Hemostasis Disorders

A

Thromboembolic Disorders
▪ Excessive clotting – thrombus vs. embolus
▪ D.I.C. – clotting AND bleeding disorder
▪ Rx: Aspirin (antiprostaglandin inhibits Thromboxane A2
), TPA, “kinase”
enzymes, Warfarin
▪ Bleeding Disorders
▪ Thrombocytopenia – chemo, radiation, cancer causes petechiae
▪ Impaired liver function (cirrhosis, hepatitis, and impaired fat absorption =
loss of Vit. K)
▪ Hemophilia (A,B,C) – Factor VIII deficien

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20
Q

Pericardium is:

A
  1. Superficial Fibrous layer
  2. Deep 2 layer serous pericardium
  3. pericardial cavity (liquid)

4.Visceral layer of serous pericardium ( Epicardium )

5.Myocardium

6.Endocardium

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21
Q

Vessels returning blood to the heart include:

A

Superior and inferior venae cavae
▪ Right and left pulmonary veins

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22
Q

Blood enters the heart via right atria from superior and inferior venae cavae and coronary sinus

blood enters left atria from pulmonary veins

Ventricles are the discharging chambers of the heart

Papillary muscles and trabeculae carneae muscles mark ventricular walls

Right ventricle pumps blood into the pulmonary trunk
Left ventricle pumps blood into the aorta

A
23
Q

Coronary circulation is t

A

the functional blood supply to the heart muscle
itself

24
Q

Heart valves :
AV valves:

A

Heart valves ensure unidirectional blood flow through the heart
▪ Atrioventricular (AV) valves lie between the atria and the ventricles
▪ AV valves prevent backflow into the atria when ventricles contract

Chordae tendineae anchor AV valves to papillary muscles

25
Q

▪ Heart sounds (lub-dup) are associated with closing of heart valves

A

First sound occurs as AV valves close and signifies beginning of
systole
▪ Second sound occurs when SL valves close at the beginning of
ventricular diastole

26
Q

▪ Systole –
▪ Diastole –

A

▪ Systole – contraction of heart muscle
▪ Diastole – relaxation of heart muscle

27
Q

Chemical Regulation of the Heart

A

▪ The hormones epinephrine and thyroxine increase heart rate
▪ Intra- and extracellular ion concentrations must be maintained for
normal heart function

28
Q

Regulation of Heart Rate: Autonomic Nervous System

A

Sympathetic nervous system (SNS) stimulation is activated by stress,
anxiety, excitement, or exercise
▪ Parasympathetic nervous system (PNS) stimulation is mediated by
acetylcholine and opposes the SNS
▪ PNS dominates the autonomic stimulation, slowing heart rate and
causing vagal tone

29
Q

Leukopoiesis

A

Interleukins
Colony Stimulating Factors

these both promote and stimulate division of WBC

30
Q

Myeloid Stem Cell

A

Myeloblast
▪ Monoblast

31
Q

Lymphoid Stem Cell

A

Lymphoblasts

32
Q

Hemostasis

A

1.Vasucular spasms due to injury

2.Platlet plug

  1. Coagulation : blood thickening
33
Q

Innate - Epithelial Chemical Barriers

A

Epithelial membranes produce protective chemicals that destroy
microorganisms
▪ Skin acidity (pH of 3 to 5) inhibits bacterial growth
▪ Sebum (oil) contains chemicals toxic to bacteria
▪ Stomach mucosae secrete concentrated HCl and protein-digesting
enzymes
▪ Saliva and lacrimal fluid contain lysozyme which destroys bacteria
▪ Mucus traps microorganisms that enter the digestive and respiratory
systems

34
Q

Surface Barriers

A

Skin, mucous membranes, and their secretions make up the first line of
defense
▪ Keratin in the skin:
▪ Presents a formidable physical barrier to most microorganisms
▪ Is resistant to weak acids and bases, bacterial enzymes, and toxins
▪ Mucosae provide similar mechanical barriers

35
Q

Respiratory Tract Mucosae

A

Mucus-coated hairs in the nose trap inhaled particles
▪ Mucosa of the upper respiratory tract is ciliated
▪ Cilia sweep dust- and bacteria-laden mucus away from lower
respiratory passages

36
Q

Internal Defenses: Cells and Chemicals

A

The body uses nonspecific cellular and chemical devices to protect
itself
▪ Phagocytes and natural killer (NK) cells
▪ Antimicrobial proteins in blood and tissue fluid
▪ Inflammatory response enlists macrophages, mast cells, WBCs, and
chemicals

37
Q

Mechanism of Phagocytosis

A

▪ Microbes adhere to the phagocyte
▪ Pseudopods engulf the particle (antigen) into a phagosome
▪ Phagosomes fuse with a lysosome to form a phagolysosome
▪ Invaders in the phagolysosome are digested by proteolytic enzymes
▪ Indigestible and residual material is removed by exocytosis

38
Q

Natural Killer (NK) Cells

A

Cells that can kill cancer cells and virus-infected cells
▪ Natural killer cells:
▪ Are a small, distinct group of large granular leukocytes (WBC’s)
▪ React nonspecifically and eliminate cancerous and virus-infected cells
▪ Kill their target cells by releasing perforins and other cytolytic chemicals that
attack the target cells membrane
▪ Secrete potent chemicals that enhance the inflammatory response

39
Q

Inflammation: Tissue Response to Injury

A

▪ The inflammatory response is triggered whenever body tissues are
injured
▪ Prevents the spread of damaging agents to nearby tissues
▪ Disposes of cell debris and pathogens
▪ Sets the stage for repair processes
▪ The four cardinal signs of acute inflammation are redness, heat,
swelling, and pain

40
Q

Inflammation Response

A

▪ Begins with a flood of inflammatory chemicals released into the
extracellular fluid
▪ Inflammatory mediators:
▪ Include kinins, prostaglandins (PGs), complement, and cytokines
▪ Are released by injured tissue, phagocytes, lymphocytes, and mast cells
▪ Cause local small blood vessels to dilate, resulting in hyperemia

41
Q

Inflammatory Response: Vascular Permeability

A

▪ Chemicals liberated by the inflammatory response increase the
permeability of local capillaries
▪ Exudate (fluid containing proteins, clotting factors, and antibodies):
▪ Seeps into tissue spaces causing local edema (swelling), which
contributes to the sensation of pain

42
Q

Inflammatory Response: Edema

A

The surge of protein-rich fluids into tissue spaces (edema):
▪ Helps to dilute harmful substances
▪ Brings in large quantities of oxygen and nutrients needed for repair
▪ Allows entry of clotting proteins, which prevents the spread of bacteria

43
Q

Inflammatory Response: Phagocytic Mobilization

A

▪ Leukocytosis – neutrophils are released from the bone marrow in
response to leukocytosis-inducing factors released by injured cells
▪ Margination – neutrophils cling to the walls of capillaries in the injured
area
▪ Diapedesis – neutrophils squeeze through capillary walls and begin
phagocytosis
▪ Chemotaxis – inflammatory chemicals attract neutrophils to the injury
site

44
Q

Fever

A

Abnormally high body temperature in response to invading
microorganisms
▪ The body’s thermostat is reset upwards in response to pyrogens,
chemicals secreted by leukocytes and macrophages exposed to bacteria
and other foreign substances

45
Q

Lymphocytes

A

Immature lymphocytes released from bone marrow are essentially
identical
▪ Whether a lymphocyte matures into a B cell or a T cell depends on
where in the body it becomes immunocompetent
▪ B cells mature in the bone marrow
▪ T cells mature in the thymus

46
Q

High fevers are dangerous as they can denature enzymes
▪ Moderate fever can be beneficial, as it causes

A

The liver and spleen to sequester iron and zinc (needed by
microorganisms)
▪ An increase in the metabolic rate, which speeds up tissue repair

46
Q

Interferon

A

genes that synthesis IFN are activated with a host cell is invaded by a virus
Interferons leave the infected call and enter neighboring cells
Interferon activates PKR- which blocks viral reproduction in the neighboring cell

47
Q

Antimcrobial protiens

A

Interferon : hindering microorganisms abilty to reproduce

Complement protiens - attacking microorganisims directly

48
Q

Self-Antigens: MHC (Major Histocompatibility Complex) Proteins

A

Our cells are dotted with protein molecules (self-antigens) that are not
antigenic to us but are strongly antigenic to others
▪ One type of these, MHC proteins, mark a cell as self
▪ The two classes of MHC proteins are:
▪ Class I MHC proteins – found on virtually all body cells
▪ Class II MHC proteins – found on certain cells in the immune response

48
Q

Adaptive Immune Defenses

A

▪ The adaptive immune system is antigen-specific, systemic, and has
memory
▪ It has two separate but overlapping arms
▪ Humoral, or antibody-mediated immunity
▪ Cellular, or cell-mediated immunity

49
Q

Antigen-Presenting Cells (APCs)

A

▪ Major rolls in immunity are:
▪ To engulf foreign particles
▪ To present fragments of antigens on their own surfaces, to be
recognized by T cells
▪ Major APCs are dendritic cells (DCs), macrophages, and activated B
cells
▪ The major initiators of adaptive immunity are DCs, which actively
migrate to the lymph nodes and secondary lymphoid organs and
present antigens to T and B cells

50
Q

Importance of Humoral Response

A

Soluble antibodies
▪ The simplest ammunition of the immune response
▪ Interact in extracellular environments such as body secretions, tissue
fluid, blood, and lymph

51
Q

Importance of Cellular Response

A

T cells recognize and respond only to processed fragments of antigen
displayed on the surface of body cells
▪ T cells are best suited for cell-to-cell interactions, and target:
▪ Cells infected with viruses, bacteria, or intracellular parasites
▪ Abnormal or cancerous cells
▪ Cells of infused or transplanted foreign tissue

52
Q

T cells must simultaneously recognize:

A

Nonself (the antigen)
▪ Self (a MHC protein of a body cell)

53
Q
A

Points and Channel location (16 decks)

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