Week 2 Flashcards
(116 cards)
1
Q
List the basic steps of counterstrain technique
A
- Identify tender point
- Establish pain scale (10/10)
- Place in position of ease while monitoring
- Recheck tender point (0/10)
- Monitor and hold position for about 90 seconds
- Return to neutral passively
- Recheck tender point (at least 70% improvement)
2
Q
List 4 upper extremity tender points of the anterior shoulder
A
- Pec Minor
- Biceps-long head
- Biceps-short head
- Subscapularis
3
Q
What is the action of supraspinatus?
A
Abduction
4
Q
What is the action of infraspinatus?
A
- External rotator of the shoulder
- Assist in shoulder extension and adduction
5
Q
What is the action of Pec Minor?
What is its insertion?
A
Action: Stabilize scapula drawing it inferiorly and anteriorly
Elevate ribs when scapula is fixed
Assist protraction & downward rotation of scapula
Insertion: Medial border & superior surface of coracoid process of the scapula
6
Q
What is the main action of biceps brachii:
A
- Chief supinator
- When arm is supine, some flexion
- Short head resists dislocation of shoulder
7
Q
What head of biceps brachii plays a more significant role in muscle action?
A
- Short head performs ~90% of of biceps function
8
Q
What is the action of supraspinatus?
A
- Initiates shoulder abduction
9
Q
What is the action of subscapularis?
A
- Internal rotation of the humerus
- Adduction of the arm
10
Q
What is the counterstrain positioning for Pectoralis minor treatment?
A
- Arm crossed over the chest
- Shoulder flexion with adduction and inferomedial traction
11
Q
What is the counterstain treatment position for long head of biceps brachii?
A
- Wrist supinated
- Elbow flexion and some shoulder flexion
12
Q
Which head of the biceps is more lateral? Which is more medial?
A
- Long head is more lateral, supraglenoid tubercle of scapula
- Short head is more medial, tip of coracoid process of scapula
13
Q
What is the counterstrain treatment position for short head of biceps brachii?
A
- Arm cross over chest touching shoulder
- Wrist supinated
14
Q
What is the counterstrain positioning for subscapularis treatment?
A
- Shoulder extension with internal rotation and slight adduction/abduction
15
Q
What is the positioning for counterstrain treatment of supraspinatus?
A
- Shoulder flexed with abduction and external rotation
16
Q
What is the counterstrain positioning for treatment of infraspinatus
A
- Shoulder flexion (90-120 degrees) with abduction and either internal or external rotation
17
Q
What is the counterstrain positioning for levator scapulae?
A
- Pt prone
- Slight shoulder extension with internal rotation
- Apply traction to rotate scapula spueriormedially
- Pt neck and face towards the side being treated
18
Q
What is the counterstrain treatment positioning for rhomboids?
A
- Patient seated or prone
- Shoulder extension with adduction by pulling arm posterior medially towards spine
19
Q
What is the counterstrain treatment positioning for radial head?
A
- Seated or supine
- Elbow extension with slight abduction and forearm supination
- Mild valgus at elbow
20
Q
What is the counterstrain treatment positioning for medial epicondyle?
A
- Pt seated or supine
- Elbow flexion with slight adduction and marked forearm pronation with slight wrist flexion
21
Q
What is the action of levator scapule?
A
- Sidebends the head and neck
- Elevates and rotates the scapula
22
Q
What is the action of rhomboids?
A
Stabilization
Retraction
Elevation and internal rotation of scapula
23
Q
What is the counterstrain treatment positioning for palmar wrist?
A
Flexion of wrist and elbow with slight ulnar or radial devation
24
Q
What is the counterstrain treatment positioning for dorsal wrist?
A
- Extension of wrist with slight ulnar or radial deviation of wrist as needed
25
What is the counterstrain treatment positioning for First carpometacarpal?
- Lateral thumb
- Flexion of wrist and abduction of thumb
26
What is the counterstrain treatment positioning for flexor pollicis brevis?
Flexion of wrist with flexion or adduction of thumb
Usually more medial
27
List three suspected diagnotsis that might indicate ordering an Abdominal XR
- Bowel obstruction
- Bowel perforation
- Kidney stones
28
What is Rigler's sign?
- The Rigler sign, also known as the double-wall sign, indicates the presence of free air within the peritoneal cavity (pneumoperitoneum
- seen on XR
29
What is Steinstrasse?
- Small calcifications lineraly arranged
- Can be seen in the ureter as kidney stones are excreted
30
What is a basic definition of Fluoroscopy?
- Live XR performed during administration of contrast material
31
Name 5 type of fluoroscopic studies
1. Barium swallow
2. Upper GI series
3. Barium enema
4. Small bowel follow through
5. Urologic eval for bladder mass etc.
32
When oral contrast is administered, how long to wait for CT to be performed for small bowel imaging?
~ 2-3 hours for contrast to reach the small bowel
33
Where does a barium swallow study stop?
At the gastroesophageal junction
34
Where does an upper GI study stop?
At the ligament of Treitz
35
What is the ligament of Treitz?
- a thin band of tissue (peritoneum) that connects and supports the end of the duodenum and beginning of the jejunum in the small intestine
- Forms boundary of upper GI vs Lower GI
36
What is a Schatzki's ring?
- Narrowing of GE junction
- A Schatzki's ring is a ring of tissue that forms inside the esophagus, the tube that carries food and liquid to your stomach.
- This ring makes the esophagus narrow in one area, close to where it meets the stomach
37
Chronic stricture of terminal ileum + Mucosal wall thickening =
Chron's disease
38
What are the primary targets for Abdominal U/S?
1. Gallbladder
2. Liver
3. Kidneys
4. Spleen
*5. Pancreas but not normally well viewed
39
What are some common indications for ordering RUQ U/S?
1. Epigastric pain
2. Abnormal liver enzymes
3. Renal failure
40
Why is the pancreas not well viewed on abdominal U/S?
Pancreas often obscured by gas in the stomach
Remember sound waves do not readily transmit through air
41
When is CT not an optimal indication for abdomen exam?
- Not optimal evaluation for **solid** abdominal organ or bowel pathology except kidney stone
42
What is the ideal patient parameter for CT with Oral contrast
When patient has BMI < 25
43
What is ACR appropriateness criteria?
Website providing indications for various radiologic studies
44
What is the indication for ordering CT with & without contrast?
- When trying to _characterize_ specific known pathologies such as liver mass, renal mass, adrenal mass
45
The density of liver and spleen should be about equal on CT. What might cause the liver to not match the spleen?
- If the density of the liver changes
- I.e. if there is fatty infiltrate of the liver will change density of image on CT b/c fat is less dense
46
T/F: There should be mild dilation of the pancreatic duct after meal visible on CT
False, dilation of the pancreatic duct should not be visible on CT
47
What can cause formation of calcifications in the pancreas?
Repeat acute pancreatitis can cause formation of calcifications
48
On imaging, what would you expect the appendix to measure?
Appendix should be > 8 mm
49
When there is stool impaction, what can this induce regarding the rectum?
- Causes perirectal inflammation
- Can cause ischemia of the rectum due to pressure on the bowel wall
50
Both the flexor carpi radialis and flexor carpi ulnaris originate from the medial epicondyle and flex the hand. What are their other actions
Flexor carpi ulnaris: **adducts** hand
Flexor carpi radialis: **abducts** hand
51
What is the action of flexor pollicis brevis?
Flex and adduct the thumb
52
What is the counterstrain treatment positioning for lateral trochanter (_______________________)
- IT band
- Abduction of the leg with slight flexion
- Patient prone
53
What is the counterstrain treatment position for the medial meniscus?
- Patient seated
- Knee flexed with internal rotation
- Adduction of tibia and ankle plantar flexion and inversion
54
What is the counterstrain treatment position for the lateral meniscus?
- Patient seated
- Knee flexed with external rotation
- Abduction of tibia and ankle eversion & dorsiflexion
55
What counterstrain technique has 2 locations for treatment?
Hamstring can have lateral or medial treatments
56
What is the counterstrain treatment position for the medial hamstring?
1. Patient prone
2. Marked knee flexion with internal rotation and slight adduction of tibia
57
What is the counterstrain treatment position for the lateral hamstring?
1. Patient prone
2. Knee flexion with external rotation and slight abduction of the tibia
58
What is the counterstrain treatment position for extension for gastrocnemius tenderpoint?
1. Pt prone
2. Knee flexion & Planter flexion
3. Pressure of calcaneus towards knee
59
What is the origin of quadratus plantae?
Calcaneus
60
What is the counterstrain treatment position for quadratus plantae tenderpoint?
1. Prone
2. Plantar flexion with translation of calcaneus towards the forefoot
61
What is the counterstrain treatment position for lateral ankle tenderpoint?
1. Pt prone
2. Ankle eversion with slight plantar flexion
62
What is the counterstrain treatment position for medial ankle tenderpoint?
1. Pt prone
2. Subtalar inversion
63
What is the counterstrain treatment position for navicular tenderpoint?
1. Pt prone
2. Plantar flexion of talotibial joint
3. Inversion of subtalar joint
4. Supination of forefoot
64
What are the major contributors of carbons in glucogneogenesis?
- Lactate & Pyruvate
- Gluconeogenic Amino acids
65
What are the minor contributors of carbons in gluconeogenesis?
- Glycerol (from TAG lypolysis)
- Propionyl CoA (from Odd chain fatty acid synthesis)
66
In gluconeogenesis, where does energy input come from since this is a high energy requiring process?
- Fatty acid metabolism
67
What are the main sites of of gluconeogenesis?
- Mainly in liver
- Some in kidney in late fast
68
What are the 4 major steps of gluconeogenesis?
- Pyruvate → PEP using 2 enzymes & occurring in 2 places
- Fructose 1,6-Bisphosphate using **Fructose 1,6-Bisphosphatase**
- Glucose-6-P to Glucose using **Glucose-6-Phosphatase**
69
List the 2 step process of Gluconeogenesis and converting Pyruvate back into PEP
1. Takes place in the *mitochondria* using **Pyruvate carboxylase** with the use of an ATP. Pyruvate converted to Oxaloacetate. **Requires biotin**
1a. 2 intermediate steps for the next step to be able to take place in the cytosol
2. In the cytosol **PEPCK** uses a GTP to convert Oxaloacetate into PEP that can
- Overall going from 3 carbon structure to 4 carbon back to 3 carbon structure
70
What does PC stand for in Gluconeogenesis & what does it require?
- Pyruvate carboxylase
- Requires biotin to convert Pyruvate into Oxaloacetate in the mitochondria
- Requires energy in the form of ATP
71
What does PEPCK stand for in Gluconeogenesis & What does it requires
- Posphoenolpyruvate Carboxykinase
- Requires energy input in he form of GTP
72
Consider this, lactate is going to enter the Gluconeogenic pathway. How does it get there?
- Lactate is formed in muscle (under anaerobic conditions) as well as in RBCs by Lactate dehydrogenase
- This regenerates NAD+ for glycolysis
- Lactic acid is sent to the liver to be metabolized → lactate → Pyruvate. Using lactate dehydrogenase
73
Recall that the first step of Gluconeogenesis starts in the mitochondria, describe the conversion of Oxaloacetate into Malate so that the remained of the cycle can continue in the cytoplasm
- Oxaloacetate has 2 mechanisms to leave the mitochondria for Gluconeogenesis cycle
- Oxaloacetate can be converted into Malate by Mitochondrial dehydrogenase to leave the mitochondria
- Then once in the cytosol, Malate dehydrogenase can convert Malate into Oxaloacetate which can continue in the gluconeogenic pathway
74
Recall that the first step of Gluconeogenesis starts in the mitochondria, describe how PEP can be generated to directly enter Gluconeogenesis after leaving the mitochondria
- Oxaloacetate has 2 mechanisms to leave the mitochondria for Gluconeogenesis
- When pyruvate enters the mitochondria can be converted directly into PEP by _Mitochondria PEP carboxykinase_ by utilizing CO2
- PEP can diffuse through the mitochondria and enter the gluconeogenic pathway
75
Once PEP enters Gluconeogenesis, the reverse of Glycolysis takes place until:
- Until Fructose 1,6 Bisphosphatase which is a highly regulated step
76
What is the Cori Cycle?
a metabolic pathway where lactate produced by muscles during anaerobic exercise is transported to the liver, converted back into glucose, and then returned to the muscles to be used for energy
77
Describe the intersected regulation of PFK-1 & Fructose-1,6-Bisphosphatase
Both are regulated by Fructose 2,6 Bisphosphate which is produced by PFK-2
- When Phosphorylated PFK-2 **cannot** make Fructose-2,6-Bisphosphate
- Thus for **glycolysis** which is active in FED state, PFK is **dephosphorylated** and can make F-2,6-BP to activate **PFK-1**
- For Gluconeogenesis which is active in the fasting state, PFK-2 is _phosphorylated_ and _cannot make F-2,6-BP_. Since F-2,6-BP is an INHIBITOR of Fructose-1,6-Bisphosphate then this pathway can be **active**!!!
78
What is the last step of gluconeogenesis pathway for liver & kidney?
- Converting Glucose-6-Phosphate into Glucose!
79
What is the final responsible for generating glucose in gluconeogenesis?
- Glucose-6-Phosphatase
80
Which amino acids are gluconeogenic?
All, **except** Leu & Lys
81
T/F: During gluconeogenesis, the glucose made will replenish Blood glucose for all tissues except muscle & adipose early in a fast
True
82
In a late fast, what tissues will be provided the glucose being made from gluconeogenesis?
Brain and RBCs because they are entirely glucose dependent
83
Describe how Ala can be converted to pyruvate to enter the Gluconeogenic pathway
- Alanine, an A.A. can be deaminated to produce pyruvate
- Or all amino acids, except for Leu & Lys, can enter the TCA and generate Oxaloacetate
84
Describe the intersected regulation of PDH complex (_____________________) & Pyruvate Carboxylase (__________________)
- PDH is b/t Glycolysis & TCA: Break down glucose for energy use
- PC is gluconeogenesis: Generate Glucose
- Both are regulated by Acetyl CoA which signals there is high energy status, _which high energy is needed for PC function_
- PDH is inhibited by Acetyl CoA because means there is enough to send to TCA
- PC is **activated** by Acetyl CoA
85
Fructose-1,6-Bisphosphatase (______________________) is activated by _lack of_ ___________________________ & F-2,6-Bisphosphate. It is activated by:
Fructose-1,6-Bisphosphatase is _inactivated by_ Fructose-2,6-Bisphosphatase & AMP
It is **activated** by ATP
Fructose-1,6-Bisphosphatase is in gluconeogenesis pathway
86
In long term regulation of Gluconeogenesis, what is the regulation?
- Induction & Repression of genes expressing PEPCK (phosphoenolpyruvate carboxylase kinase) that is the second step in generating PEP from pyruvate
87
What is the purpose of Hexose mannose path?
- The third pathway for glucose to take once inside the cell
- Produce lots of NAPH
- Or produce Ribose-5-P
88
There are two stages of HMP shunt:
Oxidative/Irreversible
Non-oxidative/Reversible
89
The ______________________/irreversible stage of HMP shunt generates:
- Oxidative/Irreversible
- 2 molecules NADPH per molecule of entering Glucose-6-P
- Ribulose 5-P
90
When is the oxidative/___________________________ stage of HMP active?
- Oxidative/Irreversible
- Active in the liver in well fed state
- Adrenal cortex for steroid hormone synthesis
- RBC
- Neutrophils
91
What is the first step of the oxidative/irreversible stage of HMP?
1. Glucose-6-P is broken down into 6-Phosphogluconolactone by **Glucose-6-phosphate dehydrogenase (G6PD)**
- Generates 1 NADPH
**this is the key committing and regulatory step of the process
92
What is the 2nd regulated step of the oxidative/irreversible stage of HMP?
3. 6-Phosophogluconate is transformed into **Ribulose-5-Phosphate** by 6-Phosphogluconate dehydrogenase
- Generates 1 NADPH
- Generates 1 CO2
93
What is the regulation of G6PD in __________________/_________________ stage of PPP?
- Glucose-6-phosphate dehydrogenase is regulated by one of its products, NADPH
- This is the first major step in the oxidative/irreversible stage of HMP
94
The product of the oxidative/irreversible stage of PPP is:
This product then enters the non-oxidative/reversible stage to make: 1.
2.
The product of oxidative/irreversible stage of PPP is Ribulose-5-phosphate
This product enters the non-oxidative/reversible stage of PPP and can be converted to **Ribose-5-phosphate** or intermediates of glycolysis including Glyceraldehude-3-phosphate and Fructose-6-Phosphate
95
T/F: Since HMP is such a large contributor of NADPH, both stages generate NADPH
False, only the first stage of HMP-Oxidative/Non-reversible stage makes NADPH
96
The entering molecule of the reversible/_________________ stage of HMP is converted to ______________________ that can be used to make nucleotides for rapidly dividing cells.
The entering molecule of reversible/non-oxidative stage of HMP is converted to Ribose-5-phosphate for use to build nucleotides in rapidly dividing cells like hair follicles, intestinal epithelial cells, skin cells
97
What are two important enzymes of the non-oxidative/reversible stage of HMP? What is their purpose
- Transketolase & Transaldolase
- They are involved in the interconversion of intermediates of glycolysis that can be generated from Ribulose-6-phosphate
98
Transketolase, an enzyme in the non-oxidative/reversible stage of HMP, requires what cofactor?
Requires Thiamine Pyrophosphate, Vitamin B1 coenzyme
99
What does NADPH have to do with RBCs?
- Protection against Reactive oxygen species formed in RBCs since they are in contact with so many in the blood stream and ROS are a byproduct of mitochondrial respiration
100
Superoxides can be transformed into Hydrogen peroxide. H2O2 is then transformed into water using the enzyme ____________________ _________________. Which becomes ____________________ in this process.
Superoxides can be transformed into Hydrogen peroxide. H2O2 can then be transformed into water using the enzyme **Glutathione peroxidase** which becomes oxidized in this process
101
What is 2-GSH & G-S-S-G?
They are glutathione in their reduced and oxidized form. When H2O2 is transformed into H2O the 2-Glutathione-S (Reduced) becomes Glutathione-S-S-Glutathione (oxidized) so that H202 can be reduced to be converted to water to remove reactive oxygen species
102
Give an example of an enzymatic antioxidant:
Glutathione peroxidase
103
What is the purpose of antioxidants?
- Cell's mechanism to remove free radicals and minimize injury
104
List some non-enzymatic antioxidants:
Vitamin E, C & Beta carotene
105
How does NADPH contribute to the _______________ antioxidant Glutathione peroxidase?
NADPH ensures the reduced form of the enzymatic antioxidant, Glutathione-S is available so it can be oxidized by Glutathione peroxidase
106
Glutathione is used to __________________ peroxides via the action of glutathione peroxidase
Glutathione is used to reduce peroxides via the action of glutathione peroxidase
107
What happens to RBCs if there is inability to maintain reduced glutathione?
- Superoxides build up because they are unable to be reduced
- Results in weak cell membrane and leads to cell lysis
108
What does Cytochrome P450 have to do with NADPH?
- CP-450 is involved with hormone metabolism, cholesterol synthesis, vitamin D metabolism, and detoxification of xenobiotics
- Uses 2 NADPH molecules
109
What is the relationship between WBC & NADPH?
- WBC utilize NADPH to convert O2 to superoxides which spontaneously transform into H2O2 which can attack and break down bacteria
110
The lack of NADPH can negatively effect WBC phagocytosis resulting in:
Chronic granulomatous disease which is persistent, severe, pyogenic infections because WBC do not have NADPH for respiratory burst to convert O2 into superoxide that can break down bacteria
111
NO synthetase requires __________________ to make __________ from L-arginine
The enzyme NO-synthetase requires NADPH to convert L-arginine into Nitric Oxide
112
Glucose-6-Phosphate dehydrogenase deficiency is a genetic disorder. The major inherited defect results in
- An unstable enzyme with a shorter half life
- Has normal function but short life
- Causes problems with getting rid of ROS especially in RBC
113
Most individuals with G6PD (_______________________) deficiency are asymptomatic until exposed to an oxidative stress: what is a common oxidative stress?
- Glucose-6-Phosphate dehydrogenase
- Common oxidative stress include:
- Infection with macrophages generating ROS
- Oxidant drugs such as antibiotics & Fava bens
114
T/F: Glucose 6-Phosphate dehydrogenase deficiency can induce acute acquired hemolysis but do not have Heinz bodies present.
False, Heinz bodies are present
115
Inability to produce NADPH and subsequently Reduced glutathione impacts hemoglobin, how?
- H2O2 build up leads to an increased rate of hemoglobin oxidation to methemoglobin that weakens the cell membrane
116
How are Heinz bodies formed in G6PD deficiency?
Oxidation of SH groups of proteins, like hemoglobin causes denaturation of proteins that are Heinz bodies
